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A MANUAL OF 


THE 


PRACTICE OF MEDICINE 



GEORGE ROE LOCKWOOD, M. D. 

i* 

Professor of Practice in the Woman’s Medical College of the New York Infirmary; Attend¬ 
ing Physician to the Colored Hospital and to the City (late Charity) Hospital; 
Pathologist to the French Hospital; Member of the New York Academy of 
Medicine, of the Pathological Society, of the Clinical Society, etc. 


WITH 75 ILLUSTRATIONS IN THE TEXT AND 
22 FULL-PAGE COLORED PLATES. 



PHILADELPHIA 


/ 


W. B. SAUNDERS 


925 Walnut Street 
1896. 






Copyright, 1895, by 

W. B. SAUNDERS. 


ELECTROTYPED BY 
WESTCOTT & THOMSON, PHILADA. 


PRESS OF 

W B. SAUNDERS, PHILADA. 






HORACE DENNETT 


AS A TOKEN OF RESPECT AND AFFECTION 
THIS BOOK IS RESPECTFULLY DEDICATED 

BY 


THE AUTHOR 








PREFACE. 


It has been the aim of the author to present in this 
manual the essential facts and principles of the practice of 
medicine in a concise and available form. It is hoped that 
the work will meet the requirements of those who hereto¬ 
fore have been obliged to resort to the larger works of refer¬ 
ence with which medical literature is so well supplied. 

In the arrangement of the subject-matter the admirable 
classification of Osier has been adopted with but a few un¬ 
important modifications. 

Acknowledgment of the author’s indebtedness is hereby 
made to those writers from whose articles illustrations have 
been taken for use in this manual, credit in each case being 
given in the text. The author also desires to extend his 
thanks to Mr. Thomas F. Dagney, of Mr. Saunders’ publi¬ 
cation rooms, for the preparation of the index and for valu¬ 
able suggestions of a varied character while the manual 
was going through the press. 

November, 1895. 

5 




































CONTENTS 


I. THE INFECTIOUS DISEASES. 

PAGE 

Typhoid Fever. 17 

Typhus Fever. 46 

Relapsing Fever. 51 

Small-pox . 55 

Vaccinia. 64 

Varicella. 65 

Scarlet Fever. 66 

Measles . 76 

Rubella .. . •. 81 

Epidemic Parotitis. 83 

Whooping-cough . 85 

Epidemic Influenza. 89 

Dengue . 94 

Epidemic Cerebro-spinal Meningitis. 95 

Diphtheria.102 

Erysipelas . 1 1 7 

Pyaemia .121 

Septicaemia.124 

Cholera.126 

Yellow Fever...133 

Syphilis .137 

Acquired Syphilis ..138 

Hereditary Syphilis .145 

Acute Miliary Tuberculosis.148 

Malarial Fever.15 2 

Anthrax.163 

Hydrophobia.165 

Tetanus .169 

Leprosy.•• 1 73 

Glanders.176 

Actinomycosis. 179 

Milk Sickness ...181 

Weil’s Disease.181 


II. DISEASES OF THE CIRCULATORY SYSTEM. 

1. Diseases of the Pericardium.183 

Pericarditis. 

Purulent Pericarditis. I 9 2 

7 







































8 


CONTENTS. 


Chronic Adhesive Pericarditis . , 

Tubercular Pericarditis. 

Cancerous Pericarditis . , . . 

Hydropericardium. 

Hremopericardium. 

Pneumopericardium. 

2. Diseases of the Heart. 

Hypertrophy and Dilatation . . . 

Hypertrophy. 

Dilatation . 

Acute Endocarditis. 

Malignant Endocarditis. 

Chronic Endocarditis. 

Atheroma. 

Mitral Incompetency . . 
Mitral Stenosis . . . . 
Aortic Regurgitation . . 
Aortic Stenosis . . . . 
Tricuspid Regurgitation . 
Tricuspid Stenosis . . . 
Pulmonary Regurgitation 
Pulmonary Stenosis . . . 

3. Diseases of the Myocardium . . . 

Acute Myocarditis. 

Chronic Myocarditis. 

Syphilitic Myocarditis. 

Degeneration of the Myocardium . 

Aneurysm of the Heart. 

Rupture of the Heart. 

4. Neuroses of the Heart. 

Palpitation. 

Tremor Cordis. 

Intermittent Action. 

Tachycardia . 

Brachycardia. 

Angina Pectoris. 

Pseudo-angina.. . 

Exophthalmic Goitre. 

5. Congenital Malformations. 

6. Diseases of the Arteries . . . 

Arterio-sclerosis. 

Syphilitic Arteritis. 

Aneurysm . 

Aneurysm of the Abdominal Aorta 


PAGE 

• 193 

• 195 

. I96 

. I96 

. 197 

• 197 

. I98 

. I98 

. 202 
. 206 
. 212 
. 219 
. 223 

• 225 
. 226 

• 230 

• 234 

• 239 

. 24I 

. 242 
. 242 

• 243 

• 249 

• 249 

• 251 

. 2<t2 

• 2 53 

• 2 59 
. 260 
. 261 
. 261 
. 263 
. 263 
. 263 
. 264 
. 266 
. 269 
. 271 

• 2 75 
. 277 

• 277 
. 281 
. 281 
. 291 


III. DISEASES OF THE RESPIRATORY SYSTEM. 


I. Diseases of the Larynx . . . 
Spasm of the Larynx . . . . 
Acute Catarrhal Laryngitis 
Chronic Catarrhal Laryngitis . 


292 

292 

294 

296 


















































CONTENTS. 


9 

PAGE 

Membranous Laryngitis.297 

Tubercular Laryngitis.298 

Syphilitic Laryngitis.300 

(Edematous Laryngitis. 301 

2. Diseases of the Bronchi.302 

Acute Catarrhal Bronchitis.302 

Acute Croupous Bronchitis .306 

Chronic Catarrhal Bronchitis.308. 

Chronic Croupous Bronchitis.310 

Bronchiectasis.310 

Asthma.3x3 

3. Diseases of the Lungs.3x8 

Circulatory Disturbances.318 

Congestion of the Lungs.318 

(Edema of the Lungs.319 

Pulmonary Hemorrhage.320 

Broncho-pulmonary Hemorrhage, or Haemoptysis .... 320 

Pulmonory Apoplexy.323 

Lobar Pneumonia.324 

Broncho-pneumonia.341 

Broncho-pneumonia in Adults.348 

Interstitial Pneumonia.332 

Interlobular Emphysema.335 

Vesicular Emphysema.336 

Gangrene of the Lung.362 

Abscess of the Lung.364 

Syphilis of the Lung.363 

New Growths of the Lung.^66 

Echinococcus Cysts of the Lung.368 

Tubercular Inflammations in General.369 

Tubercular Diseases of the Lung.373 

Acute Pulmonary Tuberculosis.373 

Chronic Pulmonary Tuberculosis.377 

Acute Pulmonary Phthisis.382 

Chronic Pulmonary Phthisis.386 

4. Diseases of the Pleura.400 

Fibrinous or Dry Pleurisy.400 

Pleurisy with Effusion.40} 

Purulent Pleurisy.411 

Chronic Pleurisy.416 

Tubercular Pleurisy.418 

Pneumothorax .420 

New Growths of the Pleura.424 

Hydrothorax.425 

Hsemothorax.426 

5. Diseases of the Mediastinum.427 

Lymphadenitis.427 

Mediastinal Tumors.428 

Abscess of the Mediastinum.430 

Emphysema of the Mediastinum.430 

Mediastinal Hsematoma.431 

Diseases of the Thymus Gland 431 






















































IO 


CONTENTS . 


IV. DISEASES OF THE DIGESTIVE SYSTEM. 


PAGE 

1. Diseases of the (Esophagus.• 43 2 

Acute (Esophagitis. 43 2 

Chronic (Esophagitis. 433 

Stenosis of the (Esophagus. 433 

Cicatricial Stenosis. 434 

Cancerous Stricture. 435 

Spasmodic Stenosis. 437 

Dilatations and Diverticula. 43 ^ 

Paralysis of the (Esophagus. 439 

Rupture of the (Esophagus. 439 

Varix of the (Esophagus. 439 

2. Diseases of the Stomach. 44 ° 

Acute Catarrhal Gastritis. 44 ° 

Toxic Gastritis. 44 2 

Acute Croupous Gastritis. 443 

Acute Suppurative Gastritis. 444 

Mycotic and Parasitic Gastritis. 444 

Chronic Catarrhal Gastritis . 445 

Dilatation of the Stomach. 45 2 

Ulcer of the Stomach. 45 ^ 

Cancer of the Stomach.464 

Non-cancerous Tumors of the Stomach. 47 1 

Hemorrhage from the Stomach. 47 2 

Neuroses of the Stomach .. 475 

Nei*vous Dyspepsia. 475 

Hypersecretion and Hyperacidity. 47 ^ 

Gastralgia. 477 

Nervous Vomiting. 479 

Peristaltic Unrest .479 

Rumination.480 

3. Diseases of the Intestines.480 

Morning Diarrhoea ..480 

Acute Catarrhal Enteritis.481 

Chronic Catarrhal Enteritis.483 

Phlegmonous Enteritis.486 

Pseudo membranous Enteritis.486 

Mucous Colitis.487 

Diarrhoeal Diseases of Children.489 

Acute Dyspeptic Diarrhoea.490 

Acute Entero-colitis.490 

Cholera Infantum.492 

Cholera Morbus.496 

Dysentery.497 

Acute Catarrhal Dysentery.498 

Tropical or Amoebic Dysentery.499 

Acute Croupous Dysentery.501 

Chronic Dysentery.504 

Appendicitis.505 

Acute Catarrhal Appendicitis.506 

Acute Suppurative Appendicitis.508 



















































CONTENTS. 


I I 

PAGE 

Gangrenous Appendicitis.513 

Chronic Appendicitis. 5 r 5 

Ulceration of the Intestine. 5*6 

Cancer of the Intestine. 5 21 

Cancer of the Rectum. 5 2 3 

Cancer of the Caput Coli. 5 2 4 

Cancer of the Duodenum. 5 2 5 

Non-cancerous Tumors of the Intestine. 5 2 5 

Intestinal Obstruction. 5 2 5 

Hemorrhage from the Intestine. 53 1 

Fecal Accumulation. 533 

Amyloid Degeneration of the Intestine. 53 ^ 

4. Diseases of the Peritoneum. 53 ^ 

Acute Peritonitis. 53 ^ 

Acute Peritoneal Sepsis. 537 

Acute Diffuse Peritonitis. 53 ^ 

Acute Circumscribed Peritonitis. 54 2 

Chronic Peritonitis. 545 

Chronic Hemorrhagic Peritonitis. 547 

Tubercular Inflammations of the Peritoneum.547 

Acute Tuberculosis of the Peritoneum.547 

Acute Tubercular Peritonitis. 54 $ 

Chronic Tubercular Peritonitis. 549 

Cancer of the Peritoneum.551 

Ascites. 553 

5. Diseases of the Liver. 55 ^ 

Functional Disturbances of the Liver. 55 ^ 

Circulatory Disturbances of the Liver. 559 

Diseases of the Capsule of the Liver. 5 ^° 

Acute Perihepatitis.560 

Chronic Fibrinous Perihepatitis. 5^1 

Syphilitic Perihepatitis. .... 562 

Acute Parenchymatous Hepatitis. 5 ^ 2 

Cirrhosis of the Liver. 5^5 

Atrophic Cirrhosis. 5^5 

Hypertrophic Cirrhosis. 57 ° 

Syphilitic Cirrhosis. 57 1 

Abscess of the Liver. 573 

Tubercular Disease of the Liver. 579 

New Growths of the Liver. 579 

Hydatid of the Liver. 5^3 

Fatty Liver.5^6 

Amyloid Liver .. 5^8 

Jaundice. 5^9 

Acute Febrile Jaundice. 59 2 

Catarrhal Jaundice. 59 2 

Cholelithiasis. 594 

Cancer of the Gall-ducts.602 

Diseases of the Blood-vessels of the Liver.603 

6. Diseases of the Pancreas.605 

Hemorrhage.6°5 

Acute Hemorrhagic Pancreatitis.606 






















































12 


CONTENTS. 


Gangrenous Pancreatitis. 

Suppurative Pancreatitis. 

Chronic Pancreatitis. 

Pancreatic Cysts. 

Cancer of the Pancreas. 

V. DISEASES OF THE KIDNEY. 

Congenital Malformations of the Kidneys. 

Movable Kidney. 

Anomalies of the Urinary Secretion. 

Albuminuria. 

Haematuria. . 

Haemoglobinuria. 

Pyuria.. 

Peptonuria. 

Phosphaturia... 

Lithsemia; Uricaemia. 

Oxaluria. 

Chyluria.-. 

Indicanuria. 

Glycosuria. . . • 

Lipuria. 

Acetonuria .. . 

Acute Congestion of the Kidneys. 

Chronic Congestion of the Kidneys. 

Acute Degeneration of the Kidneys . .. 

Chronic Degeneration of the Kidneys. 

Acute Exudative Nephritis. 

Acute Diffuse Nephritis. 

Chronic Bright’s Disease.. 

Chronic Diffuse Nephritis with Exudation. 

Chronic Diffuse Nephritis without Exudation .... 

Waxy Degeneration of the Kidney. 

Tubercular Diseases of the Kidney. 

Tuberculosis of the Kidney. 

Tubercular Pyelonephritis. 

Suppurative Disease of the Kidney. 

Tumors of the Kidney. 

Cysts of the Kidney. 

Pyelitis. 

Hydronephrosis. 

Nephrolithiasis. 

Perinephritic Abscess. 

VI. CONSTITUTIONAL DISEASES. 

Acute Articular Rheumatism. 

Pseudo-Rheumatism. 

Chronic Articular Rheumatism. 

Muscular Rheumatism. 

Gout ... 


PAGE 

607 

608 

608 

609 

6lO 


612 

6l2 

6l4 

614 

617 

6l9 

621 

621 

622 

622 

624 

624 

624 

625 
625 
625 
625 

626 

627 
628 
629 
632 
635 
635 

6 3 9 

647 

648 
648 
648 
650 

6 53 

655 

656 

657 

6 59 

666 


667 

675 

675 

677 

678 
















































CONTENTS. 


13 


PAGE 

Arthritis Deformans. 686 

Diabetes Mellitus. 689 

Glycosuria.. . . 696 

Diabetes Insipidus. 697 

Scurvy. 698 

Rickets . 7 GI 

Purpuric Diseases.7°4 

Symptomatic Purpura.7°5 

Purpura Rheumatica.7°5 

Purpura Haemorrhagica.7°6 

Haemophilia .7°9 


VII. DISEASES OF THE BLOOD AND THE LYMPHATIC 

GLANDS. 

Anaemia.7 12 

Secondary Anaemia.7 12 

Chlorosis.7 J 6 

Pernicious Anaemia.7*8 

Leucocytosis.7 22 

Leukaemia. 7 22 

Pseudo-leukaemia . . . ..7 2 7 

Addison’s Disease.73 1 

Tuberculosis of the Lymph-glands.733 


VIII. DISEASES OF THE NERVOUS SYSTEM. 

1 . Diseases of the Membranes of the Brain.73^ 

( a) Diseases of the Dura Mater.736 

Acute External Pachymeningitis. 736 

Acute Internal Pachymeningitis . 736 

Chronic Internal Pachymeningitis.737 

Syphilitic Pachymeningitis.73& 

G) Diseases of the Pia Mater.739 

Tubercular Meningitis.739 

Acute Non-tubercular Meningitis.74 1 

Syphilitic Meningitis.• 744 

Chronic Meningitis.744 

Meningeal Hemorrhage. 745 

2. Diseases of the Blood-vessels of the Brain.747 

Congestion.747 

Anaemia.74§ 

(Edema.749 

Cerebral Hemorrhage.749 

Embolism of the Cerebral Arteries.755 

Thrombosis of the Cerebral Arteries.75^ 

Aneurysm of the Cerebral Arteries.75§ 

Thrombosis of the Venous Sinuses. 760 

Cerebral Endarteritis. 761 

3 . Diseases of the Brain-substance. 764 













































14 CONTENTS. 

PAGE 

Cerebral Localization. 7^4 

Abscess of the Brain. 7^9 

Tumors of the Brain. 77 2 

Cerebral Atrophy in Children. 778 

Cerebro-spinal Sclerosis. 781 

General Paresis. 7 ^ 2 

Chronic Hydrocephalus. 7^4 

Syphilis of the Brain. 7^5 

4. Diseases of the Spinal Cord.788 

(a) Affections of the Meninges...788 

Diseases of the Dura Mater.788 

Diseases of the Pia Mater. 79 ° 

Acute Leptomeningitis. 79 ° 

Chronic Leptomeningitis. 79 2 

Hemorrhage into the Spinal Membranes. 793 

(b) Diseases of the Blood-vessels . .. 794 

Anaemia. 794 

Hyperaemia. 794 

Hemorrhage into the Cord. 795 

Caisson Disease. 79 ^ 

(r) Diseases of the Substance of the Cord. 797 

Acute Anterior Poliomyelitis. 797 

Anterior Poliomyelitis in Children. 798 

Anterior Poliomyelitis in Adults.802 

Subacute and Chronic Poliomyelitis.803 

Progressive Muscular Atrophy.804 

Amyotrophic Lateral Sclerosis . 807 

Bulbar Paralysis.808 

Ophthalmoplegia .810 

Lateral Sclerosis.810 

Locomotor Ataxia.813 

Hereditary Ataxia.821 

Ataxic Paraplegia.821 

Myelitis, Acute and Chronic.822 

Acute Ascending Paralysis.827 

Syringo-myelia.828 

Compression-myelitis .829 

Tumors of the Spinal Cord.830 

Brown-Sequard’s Paralysis.830 

5. Diseases of the Cranial Nerves.831 

Olfactory Nerve.831 

Optic Nerve.831 

Third Nerve.832 

Fourth Nerve.833 

Fifth Nerve.833 

Sixth Nerve.834 

Seventh Nerve.835 

Auditory Nerve. 838 

Glosso-pharyngeal Nerve. 840 

Pneumogastric Nerve.840 

.Spinal Accessory Nerve.844 

Hypoglossal Nerve.846 






















































CONTENTS. 15 

PAGE 

6. Diseases of the Peripheral Nerves.847 

Neuritis . 847 

Localized Neuritis.847 

Multiple Neuritis.850 

Neuromata.855 

Neuralgia .856 

7. General Nervous Diseases.860 

Infantile Convulsions.860 

Epilepsy.862 

Paralysis Agitans...869 

Acute Delirium.871 

Chorea.873 

Choreiform Affections.879 

Tetany.880 

Migraine.882 

Occupation-neuroses. . .884 

Neurasthenia.885 

Hysteria.887 

Sun-stroke.895 

Delirium Tremens.898 

8. Vaso-motor and Trophic Disorders.899 

Raynaud’s Disease. .899 

Acute Circumscribed (Edema.900 

Facial Hemiatrophy.901 

Myxoedema and Cretinism.902 

Scleroderma.904 

Acromegaly.904 

IX. DISEASES OF THE MUSCLES. 

Myositis.906 

Progressive Muscular Dystrophy.906 

Paramyoclonus Multiplex.908 

Thomsen’s Disease.909 

X. ANIMAL PARASITES. 

Trematodes.910 

Nematodes.911 

Ascaris Lumbricoides.911 

Oxyuris Vermicularis.911 

Anchylostoma Duodenale. .912 

Trichocephalus Dispar.912 

Trichina Spiralis.913 

Filaria Sanguinis Hominis.914 

Cestodes.915 

Echinococcus Disease .... 917 




















































































A MANUAL 


OF THE 

Practice of Medicine. 


I. THE INFECTIOUS DISEASES. 


TYPHOID FEVER. 

Definition and Synonyms.—Typhoid fever is an acute 
infectious disease caused by a specific bacillus, and is cha¬ 
racterized anatomically by lesions of the intestinal and 
mesenteric glands and by enlargement of the spleen. The 
disease runs a febrile course of three or four weeks, with a 
characteristic eruption and systemic symptoms. Synonyms: 
Typhus fever (German ); Abdominal typhus; Ileo-typhus; 
Enteric fever; Autumnal fever. 

Etiology.—Typhoid fever is one of the most widely 
spread of all the infectious fevers; it occurs in all countries 
and in all climates, though it is more frequent in the tem¬ 
perate zones. It may occur at any time of the year, but it 
is most commonly seen in late summer and in early fall, 
hence the name “autumnal fever” which has sometimes 
been applied to it. It seems to occur with especial fre¬ 
quency after hot, dry summers. 

The disease affects the sexes equally, although in hospital 
practice more cases are met with in men, because they more 
readily apply for hospital treatment. 

The disease may occur at any age, but young adults 
between the ages of fifteen and twenty-five are especially 
2 17 




l8 MANUAL OF THE PRACTICE OF MEDICINE . 

susceptible. After the age of thirty-five the disease appears 
progressively infrequent. 

There is in this disease, as in all infectious diseases, a 
great difference in personal susceptibility, some individuals 
being more readily infected than others who have been sub¬ 
jected to the same degree of exposure. In cities strangers 
are more susceptible to this fever than old inhabitants. The 
development of the disease after exposure is favored by any 
inflammatory condition of the intestine, the entrance of the 
germ into the lymphatics being favored by the epithelial 
desquamation resulting from the catarrhal process. A low 
and sickly condition of the general health does not seem to 
increase the susceptibility to infection. The disease appears 
in both epidemic and endemic forms. The epidemics are 
usually local, affecting a group of houses, an institution, or 
a part of a town. The longer the epidemic, the more diffi¬ 
cult it often is to trace the source of infection. It appears 
as an endemic disease where it had previously existed as an 
epidemic, and it is endemic in almost all large cities. The 
source of infection is with difficulty traced in endemic cases. 

The actual exciting cause of typhoid fever is now proved 
to be the infection of the patient by a specific germ known 
as the bacillus typhosus , or Eberth’s bacillus. This germ is 
a short, mobile bacillus whose length is equal to one-third 
the diameter of a red blood-cell, and having rounded bulbous 
ends which often present a shining appearance, due rather 
to alterations in its protoplasm than to spore-growth, as was 
at first supposed. In its appearance and growth this germ 
closely resembles the bacterium coli commune , or ordinary 
colon-bacillus, from which it is hard to differentiate it. The 
typhoid bacillus grows with ease in almost every kind of 
nutritive media, and it possesses extraordinary vitality. It 
may persist in drinking-water or in the soil for weeks or for 
months, and may even increase in number. It grows with 


TYPHOID FEVER. 


l 9 


great rapidity in milk without altering its appearance or taste; 
and so great is its tenacity of life that it may remain impris¬ 
oned in ice for months without losing its virulent properties. 
In the accumulations of privy-vaults and sewers it finds 
conditions most favorable for its growth and activity. 
Cultures are killed by a temperature of 6o° C., by carbolic 
acid (i : 200), and by corrosive-sublimate solution (i : 2500). 
Cultures resist drying for several days, but the growth of the 
bacilli is retarded by exposure to sunlight. 

The bacillus obtains entrance to the body through the 
alimentary canal, and enters the intestinal lymphoid tissue 
probably through abrasions of the epithelial coat. It has 
been found in the lymphoid tissue of the intestines, in the 
mesenteric glands, the spleen, the liver, at times in the blood 
taken from the rose spots, and occasionally in the urine. It 
has been found also in some of the complicating lesions of 
the disease. The bacilli are found in clusters in the intes¬ 
tinal contents and the stools of patients, and are thrown out 
from the body in this way. They are not eliminated from 
the lungs or the skin. 

Methods of Infection.—The disease is in no sense per¬ 
sonally contagious, cases of typhoid being received into the 
general wards of hospitals without risk. The bacilli being 
cast off only in the dejecta of the patient, it is from the 
stools that danger of infection arises. If the stools are 
thoroughly disinfected and the bacilli are killed, there is no 
further risk of a spread of the infection. If the stools are 
not disinfected, however, the bacilli will live and thrive in 
them, and this infected sewage, draining into water-supplies, 
will spread the disease among those who drink of such 
water. 

There are three ways by which the infection of typhoid 
may occur: 

The first method is by direct infection from stools. While 


20 MANUAL OF THE PRACTICE OF MEDICINE. 

not common, infection has occurred among attendants on 
the sick and among those who have washed the soiled 
linen of typhoid patients, the germs being transferred from 
infected hands to the food, and thus obtaining entrance to 
the body. 

The second method of infection is by contamination of 
the water-supply. This is the usual source of infection, 
and it explains the origin of epidemics of the disease that 
occur from time to time in towns, in institutions, and in 
villages. Contamination of drinking-water with filth and 
sewage will not produce the disease unless to such sewage 
is added the specific germ. Interesting investigations of epi¬ 
demics frequently show their origin in the contamination of 
the water-supply by the dejecta of a single typhoid patient, 
even though months may have elapsed between the infec¬ 
tion of the sewage and the consequent contamination of the 
water-supply. The source of contamination is most easily 
traced in small epidemics, and examples of epidemics in 
hotels, villages, and towns so traced are to be found reported 
in full in medical literature. In the same way the infection 
may be conveyed by impure ice, after the thawing of which 
the germs regain their vitality. 

The third method of infection is by means of milk, in 
which the bacilli readily thrive, and to which they are added 
by impure water used either to wash the cans or to dilute 
the milk. 

There are reports of epidemics apparently caused by eat¬ 
ing meat of diseased cattle, but this mode of infection is not 
yet definitely determined. Poor drainage, sewer-gas, and 
imperfect hygiene will not of themselves cause the disease: 
they only offer favorable conditions for the growth and 
development of the bacillus. 

Pathology.—The lesions are divided into those essential 
to, and those complicating, the disease. 


TYPHOID FEVER. 21 

Essential Lesions. —The essential lesions consist in— 
i. Changes in the lymph-glands of the intestine ; 2. Changes 
in the mesenteric glands; 3. Enlargement of the spleen. 

1. The changes in the intestinal lymphoid tissue are seen 
in both the solitary and the agminated glands, but espe¬ 
cially in the latter. They are most constant in Peyer’s 
glands of the lower portion of the ileum, and they may 
appear here alone. In about one-third of the cases the 
glands of the caecum and colon are affected. 

Congestion and Hyperplasia. —The first change consists 
in the congestion and swelling of the lymph-follicles, noticed 
on the second day of the disease. Toward the end of the 
first week there is added an increase in number of the cell¬ 
ular elements, some cells resembling the ordinary lymphoid 
cells, while others are large and round with several nuclei. 
This hyperplasia further increases the size of the gland. 
The cellular increase is not entirely confined to the gland, 
but infiltrates the mucous membrane in its vicinity, small 
isolated foci being also seen in the muscular, the sub- 
serous, and even the serous coats of the intestine. In these 
masses of lymphoid cells the bacilli are constantly found. 
This cellular increase persists during the second week of the 
disease. In very mild cases, the lesion goes no further than 
this, but resolution occurs, the congestion disappears, the 
cells undergo fatty degeneration and absorption, and the 
gland assumes again its normal appearance. 

Necrosis. —In most cases, however, the lesion progresses 
to such a degree that resolution becomes impossible. The 
swelling of the gland presses on its blood-vessels, and, cut¬ 
ting off its blood-supply, induces a condition of anaemia- 
necrosis, and in consequence of this condition and of the 
direct action of the bacilli upon the tissues the cells die 
and are cast off, either gradually, by a process of ulceration, 
or en masse , by a process of gangrene. In either case an 


22 


MANUAL OF THE PRACTICE OF MEDICINE. 

ulcer is left, the walls and floor of which are composed of 
infiltrated glandular tissue, and by the further disintegration 
of these infiltrating cells the ulcer may increase in size and 
in depth. Such ulceration may perforate through the entire 
intestinal wall, or the separation of the slough may be the 
cause of hemorrhage. The process of ulceration occupies 
the third week of the disease. 

Cicatrization. —During the fourth week the ulcer begins 
to cicatrize and the normal glandular elements are re-formed. 
In some cases an ulcer may cicatrize in some portions and 
extend in others. Cicatrization should be complete toward 
the close of the fourth week, but the ulcer may remain 
sluggish and inactive until the sixth or the eighth week. 

2. Changes m the mesenteric glands are of the same nature 
and intensity as those in the intestine, the only difference 
being that the products of necrosis cannot be thrown off, 
but form foci of softened purulent matter containing bacilli. 
Small foci may eventually be absorbed, while larger ones 
may become dry and cheesy and enclosed by a fibrous 
capsule. At any time a fresh focus may rupture into the 
peritoneal cavity. 

3. The spleen regularly becomes increased in size and 
harder in consistency. These changes proceed until the 
third week, after which the spleen becomes soft and pulpy 
and returns to its normal size. In rare cases the spleen 
becomes soft, but does not increase in size. Rupture or 
a gangrenous abscess of the spleen may occur. 

Complicating Lesions. —1. Peritonitis. —This condition 
may be caused in a variety of ways—either from perforation 
of the intestine by an ulcer, from rupture of a softened mes¬ 
enteric gland, or from rupture, abscess, or infarction of the 
spleen. In some cases no cause can be found for the peri¬ 
tonitis. 

2. Catarrhal or Croupous Enteritis. —Severe inflamma- 


TYPHOID FEVER. 


23 


tions are rare, though a mild catarrhal enteritis is com¬ 
monly seen. 

3. Parotitis .—This condition may occur during the second 
or third week, and may proceed to the formation of an 
abscess. 

4. The liver becomes hypersemic and increased in size. 
The cells become swollen and coarsely granular. There 
may be foci of lymphoid cells in the substance of the organ. 

5. The kidneys show parenchymatous degeneration of 
the cells of the convoluted tubules. In rare cases there 
may be acute nephritis. There may be small foci of infil¬ 
trating lymphoid cells which may proceed to suppuration, 
causing so-called “ miliary abscesses.” In these cellular foci 
Eberth’s bacilli are found ; they may be present also in the 
urine in these cases. 

6. The heart-muscle is soft and flabby and may be the 
seat of waxy degeneration. There may be degeneration of 
any of the voluntary muscles. In rare cases pericarditis 

with effusion of serum or of pus is found. 

7. The pharynx or the larynx is often the seat of a ca¬ 
tarrhal or croupous inflammation. CEdema of the glottis 
may occur, and ulceration of the larynx occurs in a certain 
number of cases. 

8. Lungs .—In nearly all cases there is some degree of 
hypostatic congestion. In other cases there is bronchitis 
with zones of peribronchial pneumonia. This is a serious 
lesion. Mild degrees of bronchitis are commonly seen. 
Gangrene or abscess of the lung may be found, and pleurisy 
with effusion occurs in a small number of the cases. 

There may be thrombosis of some of the larger veins , 
especially of the femoral; less frequently there is thrombosis 
of the cerebral sinuses. 

Symptoms. —As the symptoms are so complex and the 
clinical aspect of the disease so varied, it seems best to con- 


24 MANUAL OF THE PRACTICE OF MEDICINE. 

sider each symptom at first in detail, and then to give a 
general description of their clinical grouping. 

Fever .—In a typical case the temperature should run a 
self-limited course of four weeks’ duration, each week pos¬ 
sessing characteristics of its own. During the first week the 
temperature gradually mounts, higher in the evening than 
in the morning, and higher each day than on the day pre¬ 
vious. The maximum, which is reached by the end of the 
week, is between 103° and 104° F. The lowest morning 
temperature is between 6 and 8 a. m. ; the highest evening 
temperature is between 6 and 9 p. m. 

During the second week the temperature remains fairly 
stationary; there are morning remissions, but these are 
slight. 

The temperature in the first part of the third week con¬ 
tinues like that of the second week, but toward the close of 
the third week the morning remissions become more marked, 
the evening rise remaining the same. 

During the fourth week the morning remissions become 
more marked, while the evening exacerbations decrease; 
toward the close of the week the morning temperature 
becomes normal, and, the evening rise becoming progress¬ 
ively less, the evening temperature becomes also normal 
and the case is completed. 

This typical temperature is depicted on Plate 1. While 
this temperature curve is typical of typhoid fever, such a 
regular schematic chart is seldom met with in actual prac¬ 
tice, variations in the course being exceedingly common. 
The commonest variations of each week will be separately 
considered. 

Variations in the First Week. — [a) It is seldom that we 
obtain the temperature of the first few days, as the disease 
begins so insidiously that it is not until the fourth or fifth 
day, as a rule, that the patient comes under observation. 


TYPHOID FEVER. 


Plate i. 



TYPHOID FEVER. Plate 3. 



Recrudescences and a true relapse. 


















































































































































































































































































































































































































































































































































































































TYPHOID FEVER . 


25 


( b ) Some cases plunge at once into their fever, the onset 
being sudden, the temperature attaining its maximum upon 
the second or third day. This sudden onset is frequently 
accompanied by a chill. (V) In some cases the temperature 
of the first week is markedly remittent, the evening rise 
being frequently preceded by a chill and followed by sweat¬ 
ing. Such cases are difficult to diagnose from malarial fever. 

Exceptions to the Second and Third Weeks. —( a ) The tem¬ 
perature may fall to normal by lysis at the close of the 
second week. These are the cases in which the lesion in 
the glands does not progress to ulceration, (b) During the 
second and third weeks the fever may be slight—between 
99 0 and 101 0 F.—and the morning temperature may even 
be normal. This may indicate a mild attack if the other 
symptoms be mild in proportion, but if the other symptoms 
be severe the low temperature is not a good sign. These 
cases with slight fever seem especially liable to relapses. 

(c) During the third week the temperature may remain 
steadily high with but slight diurnal variations. In bad 
cases the temperature may remain steadily high, persisting 
during the fourth, fifth, sixth, seventh, and eighth weeks. 
Such cases are apt to be fatal. In some cases the temper¬ 
ature suddenly mounts up before death, reaching a height 
of 109° to 1 ii° F. (Plate 2, Fig. 1). 

Exceptions to the Fourth Week .—The temperature may fall 
somewhat toward the end of the fourth week, but may still 
continue a little elevated, running between 99 0 , ioo°, and 
ioi° F. until the sixth, seventh, eighth, or ninth week. With 
this slight, steady temperature there may be profuse sweat¬ 
ing. These symptoms seem due to unhealed intestinal 
ulcers. 

In some cases a slight evening rise of temperature to 99 0 
or ico° F. may be noticed during the fifth and sixth weeks, 
without other unfavorable symptoms. This rise may be 


26 MANUAL OF THE PRACTICE OF MEDICINE. 


due either to a depressed nervous state or to some insidious 
complication. A sudden fall in the temperature with a 
subsequent rise is significant of an intestinal hemorrhage. 
The more severe the hemorrhage the more decided the 
initial fall of temperature (Plate 2, Fig. 2). 

The further modifications in the temperature caused by 
complications, and the relapses, will be considered under 
separate headings. 

Pulse .—During the first week the pulse is full, dicrotic, 
and about 100. During the second and third weeks it 
becomes quicker and feebler in direct proportion to the 
gravity of the case. A pulse persistently over 140 is of 
serious import. In some cases the pulse is feeble without 
being rapid. The weakness of the heart’s action is of more 
consequence than mere rapidity, and may endanger the life 
of the patient, especially during the third and fourth weeks. 
In some cases there may be attacks of syncope or even 
collapse, in either of which the patient may die. In other 
cases the feebleness of the heart allows of venous conges¬ 
tion and cyanosis, which further endanger the life of the 
patient. From the poor circulation thrombi may occur in 
any of the larger veins. A sudden marked increase in the 
rapidity and feebleness of the pulse indicates, as a rule, 
perforation or hemorrhage. 

Gastro-intestinal Symptoms .—The appetite is lost early in 
the disease, and does not return until convalescence. 

The tongue at first is moist and coated. In severe cases 
it has a tendency to become dry, due rather to the severity 
of the disease than to the fever. In very severe cases the 
tongue becomes dry and brown, and brownish crusts, or 
sordes, collect upon the teeth and gums, interfering with 
articulation and deglutition. This is a bad sign. 

The pharynx is usually inflamed during the first week of 
the disease. 


TYPHOID FEVER. 


2 ; 


Nausea and vomiting may occur at any time in the dis¬ 
ease, but they are not usually severe if the diet and medi¬ 
cation be judicious. In some cases, however, vomiting is 
so severe as to interfere with the feeding of the patient, and 
it may even cause death by exhaustion. 

Diarrhoea is usually present, although in some places, as 
in New York, and in certain epidemics constipation is the 
rule. The diarrhoea depends less upon the extent of the 
ulcerations than upon the severity of the associated enteritis, 
and it is rarely marked until after the beginning of the 
second week. It may last a few days only or may continue 
throughout the disease, or it may alternate with constipation. 
The stools are abundant, thin, offensive, and of a grayish- 
yellow color, and are described as suggestive of pea soup. 
It is a true fecal diarrhoea, resembling the normal contents 
of the small intestine. The passages vary in number from 
two to five daily, more frequent passages being rare. The 
common occurrence of constipation as a symptom must 
always be borne in mind. 

Tympanites develops in the second week in a great 
majority of cases, and it is due to paresis of the inflamed 
intestinal wall interfering with peristalsis. Tympanites 
usually causes bulging of the abdominal wall, although in 
some cases rigidity on palpation is alone detected. When 
once developed it is apt to persist throughout the disease. 
In moderate degree it does no more actual harm than to 
render the patient uncomfortable, but if excessive it dis¬ 
places the diaphragm upward, interferes with the action of 
heart and lungs, excites nausea and vomiting, and increases 
the danger of perforation. Tympanites is a sign of serious 
import. 

Pain and tenderness over the abdomen are commonly ob¬ 
served, and are usually more pronounced in the right iliac 
fossa. These symptoms are of no diagnostic significance. 


28 MANUAL OF THE PRACTICE OF MEDICINE. 

Gurgling in the right iliac fossa is too common in other 
diseases to be distinctive. 

Hemorrhages from the bowels are a serious symptom. 
It is important to distinguish the sources of bleeding. 

(1) There may appear slight hemorrhages during the 
first ten days of the disease, coming not from ulcers, for 
none exist at so early a date, but from the congested 
mucous membrane. They are trifling in amount, and indi¬ 
cate merely a severe degree of complicating enteritis. 

(2) The characteristic hemorrhages of the disease occur 
after the close of the second week, and are caused by the 
separation of the sloughs from the intestinal ulcerations. 
They occur in about 5 per cent, of cases, and are always 
of grave significance, for not only is the hemorrhage fre¬ 
quently fatal in itself, but it also denotes extensive and deep 
intestinal ulceration. The hemorrhage varies in amount 
from a few drops to several pints or more. When once a 
hemorrhage has occurred, others are liable to follow. The 
blood passed by the rectum may be fluid and red, or dark 
and clotted, or even tarry in appearance, according to its 
amount and the length of time it has been retained in the 
bowel. In some cases of rapidly fatal hemorrhage death 
may ensue before any blood at all has been passed. The 
symptoms caused by a severe hemorrhage appear suddenly 
—faintness, syncope, even collapse, a rapid and feeble pulse, 
great dyspnoea with restlessness (the so-called “air-hunger”), 
great pallor, and cold extremities. The mind, if clouded 
before, usually becomes clear and active. The temperature, 
as shown on Plate 2, Fig. 2, undergoes a fall of several 
degrees, perhaps to normal or even to subnormal, and this 
is followed usually by a subsequent rise to a higher plane 
than before the hemorrhage. From such a hemorrhage the 
patient may die in acute anaemia. In some rare cases the 
hemorrhage seems to exert a beneficial effect upon the 


TYPHOID FEVER. Plate 



i. Ante-mortem hyperpyrexia 2 . Fall in temperature after 3* Short pseudo-relapse. 

(a indicates administration of antipyrine). hemorrhage. 
















































































































































































































TYPHOID FEVER . 


29 

course of the disease. Subsequent hemorrhages may follow 
at intervals. 

(3) During convalescence there may be small repeated 
hemorrhages without other unfavorable symptoms. These 
hemorrhages come from sluggish ulcers which have not yet 
cicatrized. 

Nervous Symptoms .—During the first week headache is 
usually a pronounced symptom. It is usually dull in 
character, although in rare cases it may be severe, sharp, 
and associated with photophobia and convulsive twitchings, 
closely resembling in this respect the headache of menin¬ 
gitis. During the first week there are apt to be sleeplessness 
and restlessness at night. Associated with the headache 
there is often nose-bleed during the first week. 

During the second week the headache and restlessness 
give way to a mental apathy which is exceedingly charac¬ 
teristic. The face is utterly without vivacity, with a vacant, 
listless expression. The pupils are generally dilated. The 
patients answer questions correctly, although with apparent 
lack of effort and interest, and often respond only to re¬ 
peated and persistent questioning. If left alone, they lie 
quietly and do not seem to take any concern about them¬ 
selves. This condition of apathy is in sharp contrast to 
the animated, cheerful condition of acute miliary tuber¬ 
culosis, and is a strong point of differential diagnosis be¬ 
tween the two diseases. It is important to remember that 
in rare cases this apathy is not seen. 

Delirium is seen in the majority of cases, varying in 
degree from confusion of ideas to acute mania; it is, how¬ 
ever, less commonly seen than formerly, owing to im¬ 
proved therapeutics. During the first week there may 
occur a delirium which is apt to be acute and violent. This 
condition, however, is not common. The commonest form 
of delirium, which appears after the second week of the dis- 


30 MANUAL OF THE PRACTICE OF MEDICINE. 


ease, is of the low muttering variety, the patient lying quietly 
and talking incoherently. This form more usually appears 
only at night, although it may in severe cases last into the 
daytime as well. There may be a disposition of the patient 
to get out of bed, requiring careful watching. This delirium 
often alternates with periods of stupor which may become 
more profound, passing into semi-coma or even coma. In 
a few cases this form of delirium alternates with a more 
active and noisy variety. In many cases there appears no 
delirium at all, and the number of these cases seems to 
increase with the increasing applications of the hydropathic 
and antipyretic treatment of the disease. 

In all cases muscular prostration is noticeable from the 
first and increases with the disease. There may be mus¬ 
cular weakness of the bladder, causing retention of urine. 
The passage of urine should always be inquired about, as 
the patient may not speak of it because of the mental 
apathy of the disease. There may be weakness of the 
sphincter ani with incontinence of feces. 

In bad cases there are twitchings and automatic move¬ 
ments of the muscles, especially of the hands. These 
symptoms, frequently spoken of as “ subsultus tendinum” 
and “ carphologia,” belong to the latter part of the disease. 
In rarer cases convulsive movements and muscular rigidity 
are seen in the first week of the disease, associated with the 
acute headache already alluded to. 

Hyperaesthesia of the skin, which is occasionally met 
with, may be extreme. 

Spleen .—The spleen is almost invariably increased in 
size, the enlargement being usually appreciable by the close 
of the first week. After the third week it diminishes in 
size. In rare cases the spleen may remain normal in size 
should there be depletion by severe diarrhoea or by hemor¬ 
rhage. The enlargement of the spleen is more accurately 


TYPHOID FEVER. 


3 * 


determined by palpation than by percussion, as the splenic 
area is apt to be obscured by tympanites. In the majority 
of cases the spleen is tender on palpation. 

Urine .—The urine shows during the first week the changes 
commonly seen in fever, being concentrated and depositing 
urates on cooling. During the course of the disease it is 
apt to contain a little albumin and casts from parenchyma¬ 
tous degeneration of the kidney, which degeneration, how¬ 
ever, is never very severe. Ehrlich describes a color reac¬ 
tion which he considers characteristic of typhoid fever. 
To employ the test two solutions are prepared, one a per 
cent, solution of sodium nitrite, the other a per cent, 
solution of hydrochloric acid saturated with sulphanilic 
acid; 40 parts of the first solution are mixed with 1 part of 
the second, and equal parts of this mixture and urine are 
thoroughly shaken in a test-tube. Upon the addition of 
ammonia a brownish-red reaction is observed, whereas in 
normal urine a brownish-yellow, without any reddish, tinge 
is observed. This reaction is not obtained after the third 
week of the disease; but, while present during the earlier 
stages of the fever, it is not considered a pathognomonic 
test, as it may be seen in other diseases, such as acute 
tuberculosis or measles. 

Eruption .—The eruption of typhoid fever is very charac¬ 
teristic. It consists of small round spots, about pin-head 
in size, of a rose-pink color which disappears on pres¬ 
sure, the spots being slightly elevated. In severe cases 
they may be hemorrhagic. They appear usually from the 
seventh to the twelfth day, although they may be seen as 
early as the third and as late as the twentieth day. They 
are present in typical relapses. They appear in successive 
crops, each crop lasting two or three days, but they do not 
appear after the third week. They usually are seen on the 
abdomen, but may be found on the chest, thighs, and back 


32 MANUAL OF THE PRACTICE OF MEDICINE. 

as well, and in rare cases may be more generally distributed. 
The eruption is usually scanty. There may be only two or 
three spots, and unless care is exercised they may be over¬ 
looked entirely. 

Course of the Disease.— Incubation .—The period of 
incubation lasts a week or ten days, during which time there 
are apt to be indefinite symptoms—headache, lassitude, and 
slight digestive disturbances. These symptoms are neither 
characteristic nor well marked. 

The onset is usually gradual, so that it is hard to tell 
exactly the first appearance of the disease; in practice, 
however, the first noted advent of fever is considered the 
definite time of onset. 

During the first week the temperature rises from day to 
day; there are sore throat and probably epistaxis, dull 
headache with sleeplessness and restlessness, possibly a lit¬ 
tle wandering at night, and a slight apathetic condition dur¬ 
ing the day. The appetite is wholly lost. There may be 
nausea or vomiting; the bowels may be either loose or con¬ 
fined. The pulse varies from 80 to ioo and is of fair force. 
By the end of the week the spleen is felt enlarged and the 
eruption appears on the abdomen. Patients differ consider¬ 
ably as to the severity of these symptoms and as to their 
reaction to them, some patients being much prostrated, 
while others even well advanced in the disease are around 
and out. These “walking cases” are more usually seen in 
hospital practice, and they greatly increase the mortality 
rate. These walking cases may not come under observation 
until hemorrhage or perforation has occurred. 

Occasionally the onset is more acute. (<?) In some * 
cases the disease begins with a chill and a rapid rise of tem¬ 
perature. (b) In other cases there appear acute nervous 
symptoms resembling those of meningitis—headache, pho¬ 
tophobia, rigidity of the neck, and muscular twitching. ( c ) 


TYPHOID FEVER. 


33 


In other cases the onset of the disease is accompanied by 
severe bronchitis, which renders the diagnosis between 
typhoid fever and acute tuberculosis one of great difficulty. 
( d ) In other cases the disease may be ushered in by severe 
nausea and vomiting, while in rare cases the symptoms of 
acute nephritis, with smoky urine containing albumin a-nd 
casts, are the first observed. 

During the second week the symptoms become aggravated; 
the temperature remains steadily high, and the headache 
gives way to mental apathy. There may be at night sleep¬ 
lessness and slight delirium, which in severe cases continues 
at intervals into the day. The pulse is a little more rapid 
and feeble. The eruption is more apparent. The lips and 
tongue are apt to be dry. Prostration becomes more and 
more marked. There may be diarrhoea or constipation. 
There is apt to be meteorism. At the close of the week 
the patient may die with severe nervous symptoms or from 
an early hemorrhage or from perforation, while very mild 
cases may defervesce. These mild cases defervescing at the 
close of the second week are frequently spoken of as 
“ aborted typhoids,” and constitute the set of cases in 
which the intestinal lesion does not progress to ulceration. 

During the third week the temperature remains high, but 
the morning remissions become more marked. The pulse 
is more rapid and feeble, with a tendency to heart failure in 
severe cases. Cerebral symptoms are prominent, the apathy 
alternating with muttering delirium. Emaciation and 
prostration are extreme. The tongue becomes dryish. 
There may be retention of urine and incontinence of 
feces. During the third week there is danger of perfora¬ 
tion, peritonitis, hemorrhage, and pulmonary complications. 

During the fourth week the temperature finally reaches 
the normal, the pulse becomes stronger, cerebral symptoms 
disappear, the tongue becomes moist and clean, and the 
3 


34 MANUAL OF THE PRACTICE OF MEDICINE. 

patient complains only of hunger and weakness. In some 
cases the fourth week may show no improvement over the 
third, but the symptoms will continue into the fifth, sixth, or 
seventh week without mitigation. At the end of this time 
the symptoms may improve and the patient recover, or they 
may become more pronounced and lead to a fatal termina¬ 
tion. In other cases the temperature begins to fall in the 
fourth week, but does not quite come down to normal, the 
patient continuing with a slight irregular fever for from one 
to three weeks longer. In severe cases this fever is ac¬ 
companied by a continuance of general symptoms to 
some degree, the protraction of convalescence being due to 
unhealed intestinal ulcers. In others, although the fever 
continues in this way, the general symptoms rapidly dis¬ 
appear, and the patient improves daily. These cases seem 
due to post-febrile anaemia or to nerve-exhaustion. 

Insidious Cases .—Besides this regular form we find cases 
of an irregular type. These cases are usually seen in 
epidemics of some size, and they run an insidious course. 
The pulse is but slightly affected, and the temperature is 
but slightly increased, varying between 99 0 and ioo° F. In 
rare cases there is no fever. Headache, restlessness, sleep¬ 
lessness, and prostration are noticed. There may be diar¬ 
rhoea or constipation, but the enlargement of the spleen and 
the eruption are the only marked characteristic symptoms. 
These cases may not be sick enough to be in bed, or even 
in the house; the course is about four weeks, and while the 
prognosis is generally good, such light cases are as liable 
as the severer forms to hemorrhage and perforation. 

Typhoid in Children .—Typhoid fever in children differs 
from that in adults in that there is less danger of hemor¬ 
rhage or perforation, the pulse is more apt to be rapid and 
feeble, the cerebral symptoms are more prominent, and the 
temperature reaches its maximum earlier in the disease, 


TYPHOID FEVER. 


35 


is more remittent (hence often called “ infantile remittent 
fever ”), and often falls by crisis. The eruption is frequently 
slight or absent. 

Typhoid in the Aged .—Typhoid fever in the aged runs an 
insidious and frequently a fatal course. The temperature 
is not so high as in adults, but the cerebral symptoms and 
prostration are more marked. Hypostatic pneumonia, 
heart failure, and nephritis are frequent complications. 

Complications .—Perforation of the intestine, which is a 
most serious complication, occurs in 6 per cent, of cases. It 
is rare before the third week, although it has been noted on 
the eighth day. It may occur in convalescence. It is more 
apt to occur in severe cases frequently associated with hem¬ 
orrhage. It seems to be favored by meteorism, vomiting, 
and dietetic errors. The intestinal contents entering the 
peritoneal cavity, there results perforating peritonitis. 

In very severe perforations the first symptom is pain in 
the abdomen, followed by a lowering of the temperature 
with a subsequent rise, collapse, and death in a few hours, 
the condition of peritoneal septicaemia being produced. In 
less severe cases there is time for the production of a puru¬ 
lent peritonitis, which runs a course with typical symptoms, 
or, should the patient already be severely ill, the abdominal 
symptoms will be less marked, there may only be an increase 
of temperature, a more rapid and feeble pulse, and a hastened 
fatal termination. Diagnosis in such cases is difficult, espe¬ 
cially if there previously existed abdominal tenderness and 
tympanites. Peritonitis with the above symptoms is also 
seen as the result of any of the other causes mentioned 
under the head of lesions. Such a non-perforative peritonitis 
runs a longer course and may be recovered from. 

The other complications of typhoid are various, and only 
a brief mention of the most important can be made. 

The pharynx is often inflamed in the first week. Otitis 


36 MANUAL OF THE PRACTICE OF MEDICINE. 

media may occur at any time. Parotitis may occur in the 
third or the fourth week and may proceed to suppuration. 

The larynx maybe the seat of a catarrhal inflammation or 
of ulceration. There may be oedema of the glottis or peri¬ 
chondritis of the arytenoid cartilages. 

Bronchitis is common at any time of the disease. 

Broncho-pneumonia and hypostatic pneumonia are seen 
in severe cases. They add but few subjective symptoms, 
being marked by the regular symptoms of the disease and 
by the apathetic condition of the patient. The temperature 
is apt to be raised, the pulse becomes weaker and quicker, 
and the physical signs are present. 

Lobar pneumonia, gangrene of the lung, and pleurisy with 
effusion are occasionally seen. 

Thrombosis of the femoral vein is frequently seen, accom¬ 
panied by pain and oedema and by the cord-like feeling of 
the vein. 

Catarrhal or croupous enteritis or colitis may occur in 
severe degree. 

Albumin and casts are usually present in the urine in 
small amounts, from a mild form of acute degeneration of 
the kidney. Less frequently there is an acute exudative 
nephritis with diminution in the amount of urine and con¬ 
siderable amount of albumin and casts. In rare cases the 
urine may be suppressed. When the kidney is involved in 
this way there are not apt to be uraemic symptoms, but the 
temperature and pulse are affected for the worse, and the 
patient is apt to do badly. 

Subcutaneous or subperiosteal abscesses may develop, in 
the latter case frequently associated with caries of the bone. 
In these abscesses Eberth’s bacilli are found. 

Malarial infection may complicate typhoid fever at any 
time. During the course of the fever the added infection 
gives a remittent character to the temperature curve, while 


TYPHOID FEVER. 


37 


if the malarial infection show itself during convalescence, 
the temperature is more characteristic, being markedly re¬ 
mittent or even intermittent. Examination of the blood 
shows the presence of the malarial organism. 

Relapses and Recrudescences.—Relapses are seen in 
from 3 to 18 per cent, of the cases, varying in the different 
epidemics. A relapse is a second attack of typhoid with 
a repetition of the symptoms of the first attack, and is pro¬ 
duced by a reinfection of the intestine from sloughs derived 
from some part above. The intermission between the 
original attack and the beginning of the relapse may extend 
to twenty-five days, the usual period being from five to 
eight days. It is not necessary to have an intervening 
period without high temperature, as the relapse may occur 
in the fourth week, before the temperature comes down to 
normal. There may be only one relapse or there may be 
several, becoming progressively milder and occurring at 
longer intervals. The symptoms appear sooner and are 
of shorter duration than those of the primary attack. The 
temperature attains its maximum on the third to the fifth 
day; the eruption is scanty, and as a rule appears on the third, 
fourth, or fifth day. The other symptoms are much less 
severe than those of the primary attack. The duration of 
the relapse is usually from ten to fourteen days, although it 
may last as long as thirty-nine days. 

The conditions predisposing to relapse are not known, 
although it seems as if constipation were a predisposing 
factor. 

Relapses are to be distinguished from the so-called 
“ recrudescences,” or temporary rises of temperature, of 
convalescence. These rises usually occur from dietetic 
errors or from over-exertion. We have a rise of tempera¬ 
ture occurring suddenly and remaining for from one to five 
days without the enlargement of the spleen or the eruption. 


38 MANUAL OF THE PRACTICE OF MEDICINE. 

These recrudescences do not add any element of danger: 
they only retard convalescence by just so much. Plate 2, 
Fig. i, shows the temperature of recrudescence alone, 
and Plate 3 shows the temperature of recrudescence and 
relapse. 

Convalescence is always slow and tedious, usually re¬ 
quiring months before the patient is in robust health again. 
Convalescence may be interrupted in several ways. There 
may be an irregular fever which will last for several weeks. 
There may be perforation or hemorrhage or peritonitis 
during convalescence. The mind may remain feeble for 
days or weeks. Some patients can hardly be said to con¬ 
valesce at all, but remain feeble, emaciated, and anaemic, 
and die exhausted, the autopsy usually revealing extensive 
cicatrices. There may be peripheral neuritis with paralysis 
of groups of muscles. Gastro-intestinal symptoms may per¬ 
sist—vomiting, diarrhoea, or dysentery. The hair usually 
falls out during convalescence, but grows again. 

The prognosis varies in hospital and private practice 
and in various epidemics. The mortality in mild epidemics 
is from 5 to 15 per cent.; in hospital practice, from 15 to 25 
per cent. In the German military hospitals, when the 
patients are young and vigorous and are treated early, the 
mortality is from 1 to 8 per cent. A guarded prognosis 
must always be given, as mild cases may turn out badly 
and serious cases may recover. The liability to perforation, 
peritonitis, or hemorrhage lends unknown factors to each 
case. As a rule, patients with high and continuous temper¬ 
ature, or with an early involvement of nervous centres, as 
shown by muttering delirium with muscular tremors or with 
excessive meteorism and diarrhoea, are apt to do badly. 
The earlier a patient is treated and sent to bed, the better 
the prognosis. Fat, elderly people and those addicted to 
alcohol stand the disease badly. Perforation and peritonitis 


TYPHOID FEVER. 


39 


are nearly uniformly fatal. Recovery from a relapse is to 
be expected, as the symptoms are rarely severe, and per¬ 
foration, hemorrhage, and peritonitis are infrequent. 

Treatment.— Prophylactic .—Typhoid fever is largely a 
preventable disease, and the prophylactic treatment consists 
in destroying the germ where it is known to exist, and in 
preventing its admission to the human body. To accom¬ 
plish the first object the following rules should be rigor¬ 
ously obeyed, and be persisted in until convalescence is 
thoroughly established : 

The bed-linen and the clothes of the patient must be 
boiled for at least half an hour after being soaked in a strong 
antiseptic solution. The following are types of the disin¬ 
fectant solution to be employed: 

1 ^5. Bichloride of mercury, 3ij; 

Potassium permanganate, 3ij ; 

Water, I gallon.—M. 

Chloride of lime (best quality), 3iv; 

Water, i gallon.—M. 

Those washing or handling soiled bed-linen must cleanse 
their hands frequently in one of these solutions, especially 
before eating. 

The intestinal discharges and the vomited matters must 
be mixed thoroughly with sufficient disinfecting fluid for at 
least half an hour before being emptied from the vessel. 
From time to time disinfecting fluid must be poured down 
water-closets or privy-vaults. The discharges must not be 
emptied into any privy-vault that is near the water-supply. 

The nates of the patient must be cleansed and disinfected 
thoroughly after each defecation. 

To prevent the admission of the germ into the body the 
drainage, the sewage, and the water-supply must be sani- 


40 MANUAL OF THE PRACTICE OF MEDICINE. 

tary. The source of every epidemic should be traced in the 
most painstaking manner, and means should be taken to 
avert future infection. During an epidemic drinking-water 
and milk should be boiled, and care should be exercised 
that ice taken from polluted water is not used. With 
perfect disinfection of the dejecta and with perfect drainage 
not allowing pollution of water-supplies, typhoid fever 
should never occur. 

General Management .—The patient should be put to bed 
as early as possible, and be kept there until convalescence 
has been established for one week. The use of the bed-pan 
and urinal should be insisted on. The room should be 
large, airy, and moderately cool. Care should be taken to 
prevent bed-sores by keeping the sheets smooth and clean 
and by washing the patient’s back morning and night with 
alcohol and tannic acid, and after careful drying dusting it 
with starch-powder or with bismuth. The mouth and the 
teeth should be kept scrupulously clean, to avoid infection 
of the middle ear and of the parotid gland. Moreover, by 
cleansing the mouth the liability to pneumonia and stomach 
fermentation is much lessened. For this purpose listerine 
and water (i : 8) or boracic-acid solutions (i : 24) are of ser¬ 
vice. The services of a good nurse should be obtained, as 
nursing is one of the most important factors in the treat¬ 
ment of the case. In severe cases two nurses are necessary. 

The diet should be fluid and easily digestible, milk being 
the ideal food. If given properly, there are but very few 
patients who cannot take it. From three to four pints 
should be given in the twenty-four hours, in divided quanti¬ 
ties at short intervals. As a practical rule, a glassful every 
two hours in the day and when awake at night will guide its 
administration in the majority of cases. Personal attention 
must be given to the feeding of the patient to know exactly 
how much is taken and how well it is borne. In case pure 


TYPHOID FEVER. 


41 


milk is not well borne, as shown by nausea or vomiting, or 
by the finding of undigested curds in the stools, the milk 
should be reduced in quantity or be diluted with lime-water 
or any of the aerated waters, or should be peptonized. In 
case these measures fail, the patient may be fed with koumiss 
or with matzoon. In the rare cases in which milk cannot be 
taken at all the reliable preparations of beef peptonoids, beef 
tea, white of egg with water, Nestle’s food, etc. may be given 
in its stead, although they are to be avoided if possible. 
Alcohol should not be given as a routine treatment, but only 
when especial indications for it arise. 

Medical Treatment .—As there is no specific drug capable 
of exerting a direct cure for the disease, the treatment is 
mainly an expectant one, controlling those symptoms that 
exert a baneful effect on the patient, threaten his recovery, 
and cause him discomfort. The only internal treatment that 
seems to be of any service is the use of intestinal antiseptics 
for disinfecting the alimentary tract, to prevent fermentation 
and tympanites, and to guard, if possible, against auto-infec¬ 
tion and relapses. The drugs used are salol, / 9 -naphthol, 
bismuth salicylate, and creosote, and high enemata of weak 
tannic-acid solutions. These measures seem in some cases 
to be of service. Except for these, the treatment is entirely 
symptomatic. 

Fever .—In the treatment of the fever there exists a diver¬ 
sity of opinion, some recommending its reduction as soon 
as a moderate point is reached (102.5 0 F.), others preferring 
the temperature to run its own course unless it reaches too 
high a degree (105° to 106° F.). It is certain that the mor¬ 
tality of typhoid has been lessened materially by antipyretic 
treatment, and that whereas a few patients seem to be no 
worse for their fever, in the great majority of cases the re¬ 
duction of the fever is accompanied by an improvement of 
all the symptoms. It seems, then, that the best treatment 


42 


MANUAL OF THE PRACTICE OF MEDICINE. 


is to keep the temperature reduced, provided this can be 
done without harm or risk to the patient. The best method 
of doing this is by the use of hydrotherapy, first insisted on 
by Brand, but modified to suit individual cases, no strict 
rule being rigorously applied. 

Brand’s original method consists in the immersion of the 
patient in a bath of 6o° F. for fifteen minutes, repeated every 
three hours so long as the temperature is 102.2° F. by the 
rectum. During the bath cold water is applied to the head 
and the surface of the body is briskly rubbed. After the 
bath the patient is dried, wrapped in blankets, and given a 
hot alcoholic drink if chilliness is apparent. No internal 
antipyretics are employed. 

Under the Brand treatment it is claimed that not only is 
the temperature reduced, but that there is also a tonic effect 
produced on the circulatory and nervous centres, the 
intellect becomes clearer, the stupor less marked, muscular 
twitchings disappear, and insomnia is lessened, the patient 
frequently falling into a refreshing sleep. Complications are 
rendered more infrequent, and, what is most important, the 
mortality is reduced to a minimum. Brand’s latest statistics 
show but twelve deaths in 1223 cases, a mortality of but I 
per cent. Not a patient died who came under treatment 
prior to the fifth day. These statistics, however, are taken 
from German military hospitals, where the patients are 
young, robust, and are treated early. Ordinarily, under this 
treatment the mortality is about 7 per cent. No effect is 
claimed in reducing the duration of the disease nor in less¬ 
ening the liabilty to relapses. The contraindications are 
intestinal hemorrhage, perforation or danger of perforation, 
and peritonitis. Bronchitis and pneumonia do not prevent 
the treatment. 

While this extreme method maybe applicable in military 
hospitals and in robust, insensitive patients, its rigorous 


TYPHOID FEVER. 


43 


employment in all cases has decided disadvantages and 
requires modification. As a general rule, then, the modi¬ 
fied bath must be employed, the temperature being 8o° to 
90° F. at the commencement and being gradually reduced 
io° F. by the addition of cold water. This bath should 
be given whenever the temperature is 102.5 0 F. or over, 
provided it be not more frequent than every three hours. 
Friction of the body and affusion of the head should be 
employed in all cases. 

For nervous, sensitive patients who are in mortal dread 
of such a modified bath the wet pack may be employed. 
The bedding being protected by a rubber blanket, the 
patient is wrapped in wet sheets closely applied by brisk 
friction. From time to time the patient is sprinkled with 
cool water. 

The most simple method of hydrotherapy is the sponging 
of the body with water or with water and alcohol. If done 
for ten or fifteen minutes this will cause a slight reduction 
in temperature, but the method is too inefficient to be of 
much benefit in severe cases. 

The use of internal antipyretics is attended by many dis¬ 
advantages, and is less frequently employed now than for¬ 
merly. While the temperature may be reduced by these 
drugs, there is also a depression of the nervous and circula¬ 
tory centres, so that stimulants may be required to over¬ 
come the effects of the drugs. The actual mortality seems 
to be slightly increased by their use. The drugs most fre¬ 
quently employed for this purpose are antipyrine (gr. x), 
phenacetine (gr. v), and antifebrine (gr. ij). They were 
formerly given in much larger doses than at present. Qui¬ 
nine is now given, not to reduce temperature, but for its 
tonic effect. Whatever antipyretic is used should be given 
in small doses repeated in two hours if necessary, and not 
too great a fall of temperature should be produced, the re- 


44 


MANUAL OF THE PRACTICE OF MEDICINE. 


duction of. a degree or a degree and a half being usually 
sufficient. 

The pulse should be watched carefully, with special regard 
to its weakness rather than its rapidity. Alcohol is the best 
stimulant, in the form of whiskey or champagne, and when 
indicated must be given freely until its effect is noticed, even 
if 8 to 12 ounces of whiskey be given in the twenty-four 
hours. Strychnine may be combined with the alcohol, and 
is of service. Digitalis may also be employed. In cases 
where there is a rapid feeble pulse with marked septic 
symptoms, large rectal enemata and of intestinal disinfect¬ 
ants often are of benefit. 

Vomiting is best treated by regulating the diet. Bismuth 
and oxalate of cerium are occasionally serviceable. If vom¬ 
iting seems to be due to the tympanites, the latter condition 
should be treated. In severe cases rectal feeding may have 
to be resorted to. 

For the diarrhoea opium by the mouth or the rectum, 
with the addition of the ordinary astringent drugs, is to be 
given. The stools should be examined to see that the 
diarrhoea is not caused by undigested curds. 

Constipation is to be treated in the first week by saline 
laxatives or by castor oil. Later in the disease enemata are 
preferable, so that the bowel is emptied every second day. 

For the tympanites turpentine stupes or 5-minim doses of 
turpentine in capsule constitute the best treatment. Intes¬ 
tinal antiseptics, as salol, ^ 9 -naphthol, or creosote, may be of 
service, while the insertion of a soft rectal tube may afford 
relief. 

For hemorrhages the patient should be kept absolutely 
quiet, opium in full doses being given. The use of internal 
astringents does not seem to do good. Applications of ice 
to the abdomen may be employed. The diet should be 
restricted, although the patient may be given acid drinks 


TYPHOID FEVER. 


45 


and cracked ice. In case of severe hemorrhage external 
warmth and stimulants should be used. Subcutaneous in¬ 
jections of warm sterilized saline solutions may be given. 

The treatment of perforation is that, in the first place, 
of collapse—by warmth to the body and free stimulation, 
while opium should be given in full doses. Should the 
perforation occur in a robust person or during convalescence, 
the question of laparotomy and closure of the perforation 
should be considered. 

Peritonitis is to be treated by the cold abdominal coil and 
by opium in full doses. In selected cases laparotomy and 
drainage may be resorted to. 

The nervous symptoms are best controlled by the hydro¬ 
pathic treatment, which, acting as a tonic on the nervous 
centres, reduces the restlessness, allays the delirium, and 
promotes sleep. Where this treatment can be employed 
drug sedatives are seldom needed. Where drugs are needed 
phenacetine (gr. v, q. 3 h.) will relieve the headache and 
restlessness, sulphonal (gr. x-xx) or chloralamide (gr. x-xv) 
will promote sleep. In severer cases opium may be neces¬ 
sary. 

Complications are to be treated on general principles. 

Treatment of convalescence is trying to physician and to 
patient alike. The greatest care should be exercised in 
the management of the diet, as the patients are ravenously 
hungry and clamor for food. The patient should be kept 
in bed for five days after the temperature is normal, and on 
a fluid diet—not necessarily, however, on milk. No solid 
food should be given for at least ten days. At the end of 
this time one solid meal may be given in the middle of the 
day, of chop or mutton with a baked potato, and afterward 
a gradual change to three meals a day may be allowed. 
There are cases where the evening temperature remains 
irregularly high. These cases are benefited by quinine 


46 MANUAL OF THE PRACTICE OF MEDICINE. 

and solid food. During convalescence attention should be 
given to the digestion and the bowels, and tonics should be 
administered. A change of air is to be recommended, and 
patients should not be allowed to return too soon to 
business and daily cares. 

The recrudescences are to be treated by a milk diet and 
rest in bed while the fever remains high. The treatment of 
a relapse does not differ from that of the original attack. 

TYPHUS FEVER, 

Definition and Synonyms.—Typhus fever is an acute 
contagious disease with an acute onset, a characteristic 
eruption, and a febrile movement of about two weeks’ dura¬ 
tion. Synonyms: Cerebral typhus; Exanthematic typhus; 
Spotted, Camp, Jail, or Ship fever. 

Etiology.—Typhus fever is endemic in England, Ireland, 
and Russia, and to a less extent in Poland, Galicia, and cer¬ 
tain paits of Southeast Europe. A few cases occur every 
year in New York and Philadelphia. From time to time 
the disease occurs in other places in epidemics. These epi¬ 
demics have usually followed wars or famines, the disease 
being regularly favored by the overcrowding of people in 
jails, houses, or camps, by poor hygiene, by starvation, and 
by filth. It never arises spontaneously, but always from 
some previous case. It is one of the most highly conta¬ 
gious diseases known, being equally virulent throughout 
its course. The poison of the disease has not as yet been 
demonstrated, although it is known to be given off from the 
bodies of the sick and the dead, to be carried in the air, 
and to be retained in bedding, clothes, carpets, etc. for a 
considerable time, so that the poison is conveyed not only 
from person to person, but also by clothing and bed-rooms. 
But a very few persons are exempt if they be sufficiently 
exposed, and the more prolonged and concentrated the 


TYPIIUS FEVER. Plate 4. 



Chart of typhus fever (Pepper). 





















































































































































TYPHUS FEVER. 


47 


exposure the more certainly will they be attacked. One 
attack usually procures immunity. While no age is exempt, 
the majority of cases occur between the fifteenth and thir¬ 
tieth years. 

Pathology.—The eruption is the only characteristic 
lesion. After death there may be found a number of mor¬ 
bid conditions common to any of the severe infectious 
diseases. 

Symptoms.—The period of incubation is about twelve 
days, although cases may develop as early as twelve hours 
or as late as three weeks after exposure. 

The onset is abrupt, although in some cases it is preceded 
for a few days by malaise and frontal headache. The initial 
symptoms are a chill, a rise of temperature, headache, and 
prostration. The chill, which is usually sharp and severe, 
may be repeated. 

The temperature rises suddenly, attaining its maximum 
from the third to the fifth day, reaching 103° F. in mild and 
105° F. in severe cases. During the first week the tempera¬ 
ture remains steadily continuous, becoming somewhat higher 
in the second week, but with morning remissions. In bad 
cases there may be hyperpyrexia. From the twelfth to the 
fourteenth day comes the crisis, the temperature falling 
rapidly—sometimes a drop of 4 0 to 5 0 F. in a few hours, 
although usually it takes twenty-four to forty-eight hours 
before the temperature reaches the normal; this fall of 
temperature is accompanied by an improvement of all the 
symptoms, the patient entering at once upon the period of 
convalescence. 

The headache is usually frontal and is very severe—more 
so than in any other disease except meningitis. With the 
headache are pains in the back and bones and soreness of 
the muscles. 

Prostration is marked from the onset, the patient taking 











48 MANUAL OF THE PRACTICE OF MEDICINE. 

to bed from weakness within a few hours. It may be so 
severe and sudden that the patient will fall in the street 
without previous warning. 

Nausea and vomiting are commonly present, and may be 
distressing. The tongue is heavily coated in the first week, 
later having a tendency to become dry and brown, with 
sordes on the teeth and gums. The bowels are usually con¬ 
stipated, although there may be diarrhoea. 

The pulse is rapid and full, being between ioo and 120; 
it becomes more rapid and feeble during the second week. 
Marked slowness of the pulse may be observed at any time 
of the disease and may continue into convalescence. A 
drop in the pulse without improvement in other symptoms 
is not a good sign. The urine usually shows the presence 
of albumin and casts in moderate amounts from an acute 
degeneration of the kidney. More rarely there are present 
the urinary changes of acute exudative nephritis. 

Early in the disease there is a look about the patient 
which is often of diagnostic value. The face assumes a 
dusky flush, the conjunctivse are injected, and the expres¬ 
sion is dull and vacant, the whole appearance suggesting 
marked intoxication. The pupils are contracted. 

The characteristic eruption appears from the third to the 
fifth day, although it may be seen as early as the second 
and as late as the seventh day. It consists of small, irreg¬ 
ularly rounded spots, of a dirty-pink color, appearing first 
on the abdomen and chest, and becoming more general, 
although rarely seen on the face. It appears in one crop, 
and is all out in from two to five days, lasting from seven to 
ten days and then slowly fading. It is usually abundant, 
though in some cases it may be scanty. At first the spots 
are slightly elevated and disappear on pressure, but after 
several days they become petechial and more perma¬ 
nent, remaining after pressure. They have no well-defined 


TYPHUS FEVER. 


49 


margin. In children the eruption resembles that of measles, 
and from the mottled appearance given by it to the skin the 
eruption has been termed the mulberry rash. In some 
cases there is added a diffused, deep mottling of the skin 
with large purplish blotches; in others there are hemor¬ 
rhagic spots or a general erythema. These manifestations 
are not characteristic and are inconstant. 

Cerebral symptoms are marked and appear early. The 
headache, so marked at the onset, usually becomes masked 
by other nervous symptoms by the end of the first week. 
Delirium is a fairly constant symptom. In very severe 
cases it may come on in the first twenty-four hours of the 
disease in the form of an acute mania. In less severe cases 
it is not seen until the end of the first week. It may then 
be only a mild delirium at night, or it may be more decided, 
persisting throughout the day. This latter form is often 
associated with delusions which at any time may render the 
patient violent. In severe cases, during the second week 
there may be observed alternately with the delirium a form 
of deep stupor known as “coma vigil,” in which the eyes 
are wide open but the patient is unconscious. 

Deafness may appear in the second week without assign¬ 
able cause, but from it the patient usually recovers. 

If the case is to end fatally , the temperature rises, often to 
io6° or io8° F. before death, the delirium and stupor be¬ 
come more decided, there may be retention of urine and 
incontinence of feces, the pulse becomes more rapid and 
feeble, and death occurs from exhaustion from the toxaemia. 
Should the patient survive until the third week, death usu¬ 
ally results from a complicating pneumonia. 

If the case is to recover , on about the fourteenth day there 
is a decided fall in the temperature, the patient frequently 
falling into a refreshing sleep from which he awakes weak 
but convalescent. In some cases this crisis occurs as early 


4 


50 MANUAL OF THE PRACTICE OF MEDICINE. 


as the seventh day, or at this time there may be a decided 
remission in the temperature, practically an abortive crisis, 
which is to be considered a favorable omen. In other cases 
the crisis may be deferred as late as the twenty-first day. 

In some epidemics light cases are seen, running a mild 
course, with a temperature usually under 102° F., with but 
moderate cerebral symptoms. The crisis usually occurs 
between the seventh and the twelfth day. Occasionally 
there are observed in severe epidemics malignant cases in 
which the patient is overwhelmed by the virulence of the 
disease. There are rapidly developed a sudden tempera¬ 
ture, usually high, progressive heart failure, stupor, and 
coma, and death may result in from twelve to twenty-four 
hours or within two or three days. In these cases no 
regular eruption is seen, but ecchymoses and hemorrhagic 
spots are irregularly developed. 

Complications.—There may be broncho-pneumonia, 
which in rare cases is complicated by gangrene of the 
lung. Gangrene of the extremities or cancrum oris in 
children has been observed. Meningitis is rare and is 
always fatal. Abscesses in the skin and the joints may 
occur, and suppurative parotitis is not uncommon. There 
may be hemorrhages into the skin or from any of the 
mucous membranes accompanying serious cases. Throm¬ 
bosis of large veins or of cerebral sinuses may occur. 

Convalescence is usually rapid at first, although it is 
months before it is complete. There are no relapses. The 
patient may be left dull and feeble-minded, from which con¬ 
dition the recovery is gradual. A few patients develop acute 
mania in convalescence, but the ultimate prognosis is gen¬ 
erally good. Paralysis from post-febrile neuritis is not 
uncommon. 

Prognosis.—The mortality is from io to 20 per cent., 
varying with the nature of the epidemic, the previous con- 


RELAPS/JVG FEVER. 


51 


dition, and the age of the patient. The disease is rarely 
fatal in young subjects, but is very serious in those past 
adult life. Complicating inflammations alter the prognosis 
according to their nature. 

Treatment.—The patient should be isolated thoroughly 
from the start. To lessen the danger of contagion to nurse 
and to physician, the windows must be opened freely to 
admit fresh air. If possible, the patient should occupy two 
rooms, one by day and one by night, the freest ventilation 
thus being afforded. In epidemics the cases are best treated 
in tents, the patients being protected in winter by extra 
bedding. This fresh-air treatment is not only a prophylactic 
measure, but seems also to lessen the actual mortality. 
Windows should be protected by bars in case mania 
develops. 

There is no specific treatment for the disease. Formerly 
mineral acids were so considered, but they are given now 
only because they afford a pleasant acidulated drink and 
do no harm. 

The treatment, then, is entirely symptomatic. The tem¬ 
perature is best treated by hydrotherapy, as in typhoid fever, 
the bath being given as soon as the temperature reaches 
103° F. Internal antipyretics should be avoided if possible, 
because of their depressing effect. Alcohol in some form 
is demanded in almost all cases, and it may be given in 
large doses until a good effect is observed on the heart’s 
action : 10 to 20 ounces of whiskey may be required in the 
twenty-four hours. The delirium and headache should be 
treated by sedatives combined with hydrotherapy. Other 
symptoms should be treated on general principles. 

RELAPSING- FEVER. 

Definition and Synonyms.—Relapsing fever is an acute 
infectious, contagious disease due to a spirillum, and cha- 


52 


MANUAL OF THE PRACTICE OF MEDICINE. 


racterized by a febrile paroxysm of about six days’ duration, 
followed usually by one or more similar recurrences at reg¬ 
ular intervals. Synonyms: Famine fever ; Spirillum fever; 
Relapsing typhus. 

Etiology.—The disease is a rare one, occurring in epi¬ 
demics which last but a short time and then die out, leaving, 
except in very rare exceptions, no endemic cases. Epi¬ 
demics were seen in Philadelphia in 1844, and in New York 
and Philadelphia in 1847 an< ^ 1869. The last epidemic of 
any importance was in Russia in 1886. 

Epidemics have frequently been associated with those of 
typhus fever, the spread of both diseases being favored by 
filth, by famine, and by overcrowding of people. Neither 
age, sex, nor climate exerts any influence upon the epi¬ 
demics. 

The disease is actively contagious, not only by personal 
contact, but also through clothes and bedding and through 
the medium of a third person. One attack does not secure 
immunity from subsequent attacks. 

The exciting cause is infection by a spirillum or spiro- 
chaete, first described in 1873 by Obermeier. The spirillum 
is a slender spiral filament endowed with motion, its length 
being three to six times as long as the diameter of a red 
blood-cell. It is present in the blood, but only during the 
febrile paroxysm. Before the crisis and in the intervals 
between the paroxysms only round glistening bodies are 
seen, which bodies are supposed to be the spores. Inocu¬ 
lations of the spirillum into man and monkeys have repro¬ 
duced the disease. 

Pathology.—There are no lesions characteristic of the 
disease. The spleen is large and soft and may rupture. 
There are parenchymatous changes in the liver, the kidneys, 
and the heart-muscle. There may be internal hemorrhages. 
The tissues may be jaundiced. 


RELAPSING FEVER. Plate 



Typical case of relapsing fever (Pepper). 























































































































































































RELAPSING FEVER. 


53 


Symptoms.—Incubation may be short, the attack devel¬ 
oping a few hours after exposure. Ordinarily the period is 
from five to seven days, during which time there are no 
symptoms. The disease begins abruptly with a chill, fol¬ 
lowed by a rapid rise of temperature, running to 103° to 
107 0 F. within twenty-four hours. There are severe and 
distressing pains in the head, back, and bones. Prostration 
is well marked at the onset, the patient taking to his bed 
at once. The pulse is full and varies between 110 and 130. 
There is usually nausea; there may be severe vomiting, and 
in some cases vomiting of blood. In severe cases there 
may be delirium. Convulsions may be the first symptom 
in young subjects. 

The liver and spleen are regularly enlarged and tender. 
Blood-examination shows the spirilla in active movement 
among the red blood-cells. Jaundice may be present in the 
attack or in any of the relapses. It belongs to the severer 
forms of the disease. 

There is no characteristic eruption, but in certain cases 
there may appear small reddish spots somewhat resembling 
the eruption of typhus fever, or there may be petechial spots. 
The urine contains a slight amount of albumin and casts 
from parenchymatous degeneration. 

While the symptoms are at their height the paroxysm 
suddenly ceases, the temperature suddenly falling by crisis, 
and the patient is left weak but convalescent. This remark¬ 
able crisis usually occurs between the fifth and the seventh 
day, although it may occur as early as the third or as late 
as the tenth day. This abrupt crisis, which is always a 
time of danger, may be accompanied by profuse sweating or 
exhausting diarrhoea. In some cases there may be collapse, 
or hemorrhages from the stomach, the intestines, or the 
kidneys. 

After such an attack the patient may pass on to recovery, 


54 MANUAL OF THE PRACTICE OF MEDICINE. 


but in the majority of cases, after an interval of about seven 
days (the limit is from five to twenty days), the patient is again 
suddenly seized with a repetition of all the symptoms of the 
first attack, the spirilla again becoming present in the blood. 
This second attack usually is less prolonged than the first, 
lasting about three days, although it may last only one day 
or be prolonged for a week. This attack terminates by crisis 
as does the first. The patient may now pass on to complete 
recovery, or there may be a series of these relapses (up to 
five or six), these subsequent attacks becoming shorter and 
less severe. 

Complications.—There may be hypostatic congestion of 
the lungs or broncho-pneumonia. Laryngitis and oedema 
of the glottis may occur. There may be rupture of the 
spleen with internal hemorrhage and peritonitis. Nephri¬ 
tis is of rare occurrence. In severe cases there may be 
hemorrhages from the stomach, the intestines, or the 
kidneys. 

Convalescence is apt to be slow and tedious, especially 
if there has been a series of relapses. There may be paral¬ 
yses of groups of muscles from post-febrile neuritis. There 
may be ophthalmia with loss of sight. 

The prognosis is good. The mortality is from 2 to 4 
per cent. 

Treatment.—There is no specific treatment. Cases are 
to be isolated thoroughly, and clothing, etc. disinfected, to 
prevent the spread of the disease. The treatment is on 
general principles. It is especially important that the 
patient should be well watched at the time of crisis for indi¬ 
cations of heart failure. The diarrhoea which often occurs 
at this time should be treated promptly. After the crisis 
the patient should be kept in bed for at least a week and on 
fluid food. 


SMALL-POX. 


55 


SMALL-POX. 

Definition and Synonym.—Small-pox is an acute infec¬ 
tious, contagious disease with marked constitutional symp¬ 
toms and a characteristic eruption. Synonym: Variola. 

Etiology.—This disease was known to the ancients and 
was fully described by the older writers. Formerly it 
occurred in devastating plagues, but since the discovery of 
vaccination it has become less and less frequent, so that 
cases of true small-pox are but rarely seen. With universal 
vaccination the disease bids fair to become extinct. 

Small-pox is actively contagious throughout its entire 
course. The contagion, which is conveyed by personal 
contact or by the medium of a third person, emanates from 
the bodies of the sick and the dead, floats in the air, and 
can remain in bedding, clothes, cabs, and rooms for months 
and years without losing its virulent properties. It is 
inoculable by the contents of the vesicles and pustules and 
by the blood of the sick, and is most actively conveyed by 
the scales and crusts thrown off by the patients; these 
scales float in the air as a fine dust, and in this way may be 
carried long distances. 

The exact nature of the contagion has never definitely 
been determined. Micro-organisms have been found in the 
contents of the vesicles and pustules, but these micro-organ¬ 
isms are common to all suppurative processes. 

Susceptibility to the disease is almost universal except 
among those protected by vaccination or by a previous 
attack. No age is exempt, the disease even attacking the 
foetus in utero. Negroes are more susceptible than other 
races, though this may be due to their neglect of vaccina¬ 
tion. Vaccination properly performed procures immunity, 
as does a previous attack, although in rare cases the immu¬ 
nity may not extend beyond a term of years (five to fifteen). 


56 MANUAL OF THE PRACTICE OF MEDICINE. 


The disease exists in nearly all countries as an endemic 
disease, a certain number of cases occurring every year. 
Under favoring circumstances it assumes from time to time 
epidemic proportions. These epidemics are terribly devas¬ 
tating should they occur among aboriginal races where 
small-pox has not previously existed. 

Pathology.—Aside from the eruption there are no char¬ 
acteristic lesions. There may be found the enlarged spleen 
and the parenchymatous changes in the liver, the kidneys, 
and the heart-muscle that are present in all severe infectious 
diseases. Severe cases may reveal internal hemorrhages. 

Symptoms.—The period of incubation is usually from 
ten to fourteen days, during which time there are no symp¬ 
toms. 

Five forms of the disease are described: i. The discrete 
form; 2. The confluent form; 3. The hemorrhagic form; 
4. The malignant form; 5. Varioloid, or small-pox modified 
by vaccination or by a previous attack. 

1. The Discrete Form .—The symptoms are described as 
occurring in two stages. 

(a) Stage of Invasion .—The onset is sudden, being 
ushered in by a chill which is violent and severe and which 
may be repeated. The temperature rapidly rises, reaching 
103° or 104° F. in twenty-four hours. There is severe 
headache, usually frontal, which is marked and character¬ 
istic, and which lasts throughout this stage with undimin¬ 
ished severity. With the headache there are regularly severe 
pains in the bones, muscles, and loins. Especially charac¬ 
teristic is an excruciating pain in the sacrum that is present 
in about half the cases. The severity of the pains gives no 
clue to the future severity of the attack. While the head¬ 
ache and backache are common to the onset of all severe 
infections, there is no disease in which they are so marked 
as in small-pox, and their occurrence should excite appre- 


SMALL-POX. Plate 



Chart of temperature curve of small-pox (Eichhorst). 

















































































































































SMALL-POX. 57 

hension, especially during an epidemic or occurring in an 
unprotected patient who has been exposed to the disease. 

Vomiting is usually severe and distressing, and prostra¬ 
tion is an early symptom, the patient taking to his bed at 
the very onset. The pulse is rapid and full, increasing in 
rapidity with the rise of the fever, and becoming weak in 
proportion to the severity of the disease. Nervous symp¬ 
toms belong to the severer cases. There may be active 
delirium, especially in patients with high fever. Convul¬ 
sions in place of the chill may initiate the disease in chil¬ 
dren. There are usually considerable restlessness and gen¬ 
eral apprehension. The eyes are bright; the skin is hot 
and dry; the spleen is enlarged, and albumin and casts may 
be found in the urine in small amount. 

There is no characteristic eruption in the stage of inva¬ 
sion, although an initial rash may be observed. This rash 
appears with more frequency in some epidemics than in 
others, as a rule, however, appearing in from io to 15 per 
cent, of all cases. It consists of an erythema which may 
be diffuse or macular, closely resembling the eruption either 
of scarlet fever or of measles, although it differs from both 
in its localization. It is often associated with small hemor¬ 
rhagic spots. This initial erythema occurs on the second 
day, and it appears usually on the hypogastrium, the inner 
surfaces of the thighs and opposing surfaces of the side of 
the chest, and the inner side of the arms—regions which 
are usually exempt from the regular eruption. This early 
rash lasts but a short time and then fades away. 

The stage of invasion lasts regularly three days, during 
which time the symptoms continue, the temperature usually 
becoming somewhat higher, so that it may reach 105 to 

io 7 ° F. 

(b) Stage of Eruption .—The eruption is peculiar in that 
it passes through successive stages in development, becom- 


58 MANUAL OF THE PRACTICE OF MEDICINE . 


ing in turn macules, papules, vesicles, and pustules. Begin¬ 
ning on the fourth day of the disease, there appear small 
round, slightly raised spots, involving first the face, the edge 
of the hairy scalp, and the backs of the wrists, and extending 
within twenty-four hours over the trunk, the arms, and, last 
of all, the legs. On the second day of the eruption the spots 
become papules which are hard to the feel, suggesting bird- 
shot imbedded in the skin. By the third day the papules 
change to vesicles which have each a depressed iimbilicated 
centre without any tendency to rupture. Should these 
vesicles be pricked, they do not completely discharge their 
contents. Vesiculation is complete on the sixth day ; the 
vesicles then become pustular. The central umbilication 
usually disappears, so that there result pustules each with 
a rounded summit surrounded by a zone or areola of 
inflamed and swollen skin which burns and itches and 
causes the feeling of distressing tension. The face is now 
strikingly swollen and disfigured; the eyelids are closed 
by oedema. In severe cases the skin between the pustules 
becomes diffusely inflamed, adding to the distress and dis¬ 
figurement of the patient. The pustules are completely 
developed on the eighth or ninth day of the eruption, and 
after continuing for about three days begin to dry up and 
to form scabs and crusts which, falling off, leave pigmented 
spots that persist for months. If the cutis vera has been 
involved by the pustules, permanent depressed white cica¬ 
trices must necessarily result. The desiccation requires a 
week or ten days for its completion, and it is attended by 
much itching. 

There are usually similar eruptions in various mucous 
membranes, especially those of the mouth, pharynx, nasal 
cavities, larynx, and trachea, and less frequently of the 
upper portion of the oesophagus, the bronchi, the conjunc¬ 
tiva, the vagina, and the rectum. When the eruption 


SMALL-POX. 


59 


appears on mucous membranes, it is modified by the heat, 
moisture, and friction of the parts, and, instead of pustules 
being - formed, the vesicles become macerated and form 
ulcers, more or less deep, which may become confluent. 

As the eruption appears the temperature suddenly falls 
—not, however, quite to the normal, but still remaining a 
little high. The constitutional symptoms remit in their 
severity, especially the headache and backache, so that the 
patient feels quite comfortable, and often is able to leave 
the house and to apply for treatment at a hospital or a dis¬ 
pensary. 

The amelioration of the symptoms continues until the 
pustular stage is reached, when there is developed a rise 
of temperature to ioi° to 105° F. with a return of all the 
symptoms. This fever, which is termed the secondary or 
suppurative fever, is often remittent. During this stage 
there may be active delirium, so that the patient may do 
himself or his attendants bodily injury. The distress during 
this period from the itching, tension, and burning of the 
skin is almost unbearable. The patient is disfigured and 
often is hardly recognizable. 

The period of secondary fever lasts for from three 
to eight days, and then as desiccation is established the 
temperature gradually falls and convalescence is begun. 
The hair frequently falls out, and in some cases does not 
grow again. 

2. The Confluent Form .—Here the typical symptoms are 
present in the most complete development. The stage of 
invasion is short, lasting but two days as a rule. It is also 
severe, the fever being high, with pronounced headache and 
frequently with active delirium. There is no period of 
cessation with the appearance of the eruption, although the 
symptoms may remit slightly in their severity. 

The eruption is profuse, the pustules becoming confluent, 


60 MANUAL OF THE FT AC TICE OF MEDICINE. 


so that whole areas, especially of the face and hands, are 
converted into suppurating blebs. The patient is unrecog¬ 
nizable, the distress is extreme, and the stench is penetrating 
and intense. 

The mucous membranes are usually extensively involved. 
The suppurative fever is apt to run high and is attended by 
symptoms of a septic character—irregular chills followed by 
exacerbations of fever, rapid and feeble pulse, diarrhoea, and 
extreme prostration with a low muttering delirium which 
at times may assume an active form. In this septic condi¬ 
tion the patient may die. Desiccation continues into the 
third and fourth weeks, during which time the symptoms 
of the secondary fever persist with diminishing intensity. 

3. The Hemorrhagic Form .—This form is characterized by 
hemorrhages occurring in the pustules and the skin and 
from any of the free mucous surfaces—from the nose, mouth, 
lungs, stomach, intestines, kidneys, or uterus. This form 
of small-pox may occur in weak, debilitated subjects, or 
the hemorrhages may complicate the severer forms of the 
disease. 

4. The Malignant Form .—The invasion in malignant cases 
is characterized by extreme prostration and enfeebled heart- 
action, the initial rise of temperature not being high. In 
from eighteen to thirty-six hours there appears an erythema 
(resembling scarlet fever with large hemorrhagic blotches) 
which occurs extensively over the body, especially the 
abdomen and thighs. There are frequently hemorrhages 
from the mucous membranes. The regular eruption appears 
somewhat later, but does not run a perfectly typical course, 
being represented in some cases only by a few vesicles. In 
some cases death results in a few hours, before any eruption 
occurs, the patient being overwhelmed by the virulence of 
the disease. In other cases death does not occur until from 
the third to the seventh day. 


SMALL-POX. 


61 


5. Varioloid .—This disease is small-pox occurring in a 
modified form in a person who is but partially protected 
by vaccination or by a previous attack. According to 
the extent of the protection, varioloid occurs in all grades 
of severity, so that the severer grades merge into true, 
unmodified variola, while in the lesser grades the patient 
may not seem to be sick at all. No matter how trifling 
the attack may be, it is true variola, and is capable of 
causing the disease in others in even the most malignant 
forms. 

Generally varioloid runs a milder course and one of shorter 
duration than small-pox. The stage ol invasion lasts for 
two or three days. There may be a chill, with moderate 
fever, headache, pains in the back and bones, and vomiting, 
while in very light cases these symptoms may not be severe 
enough to prevent the patient from being at work and out 
of doors. 

The eruption is that of variola, but it is less abundant, 
the pustules do not reach the same size nor penetrate so 
deeply, and the areola of inflamed skin is frequently absent. 
Many of the vesicles dry up and are not converted into pus¬ 
tules. With the appearance of the eruption the fever falls 
to normal and the other symptoms of the invasion disap¬ 
pear and frequently do not return. In more severe cases 
the symptoms of the secondary fever are slight and last but 
a day or so, so that there is a striking lack of proportion 
between the appearance of the patient and the degree of 
his constitutional symptoms. Desiccation begins from the 
fifth to the seventh day, and the resulting cicatrices are 
small or are absent. 

Complications and Sequelae of small-pox are numerous, 
and are due not only to the severe infectious nature of the 
disease, but also to the suppurative foci. There may be 
laryngitis, oedema of the glottis, or necrosis of the carti- 


62 MANUAL OF THE PRACTICE OF MEDICINE. 


lages, resulting in stenosis, necessitating intubation or 
tracheotomy. 

Broncho-pneumonia is a common complication, especially 
in the severer cases. There may be pleurisy. Nephritis is 
rare, although the urine usually contains a small amount of 
albumin. There may be orchitis. During the suppurative 
stage there may be developed septicaemia or pyaemia or 
arthritis. In rare cases a disseminated myelitis has been 
observed. Convalescence may be interrupted by boils, by 
gangrene of the skin, or by erysipelas. Ulceration of the 
cornea is but rarely seen. During convalescence there 
may be a post-febrile insanity or paralyses from peripheral 
neuritis. 

Prognosis.—The prognosis depends upon the degree of 
protection afforded the patient by vaccination. Varioloid 
is very seldom fatal in those protected by vaccination, while 
in those totally unprotected the mortality ranges from 30 to 
40 per cent. The prognosis depends also upon the severity 
of the attack, the hemorrhagic and malignant forms being 
almost certainly fatal, the confluent form being very 
dangerous, while the discrete form affords a large percent¬ 
age of recoveries. It depends also upon the age and the 
condition of the patient, being most fatal in children and 
old people, in the debilitated, and in drunkards. The 
prognosis is affected also by the presence of compli¬ 
cations. 

Treatment.—If vaccination and revaccination could be 
performed thoroughly, variola would become extinct. After 
exposure to variola, revaccination should be resorted to, and 
it is probable that vaccination even in the earliest stages of 
the disease itself, if done before the fourth day, greatly mod¬ 
ifies its severity. 

Patients with variola should properly be treated in con¬ 
tagious hospitals, as few private houses afford sufficient 


SMALLPOX. 


63 


means for thorough isolation and disinfection. When this 
cannot be done, quarantine should be conducted on the 
strictest principles, and should be continued until the skin 
and the hair are absolutely free from crusts and scales. All 
articles that come in contact with the patient should be 
sterilized or be destroyed. 

The room should be kept moderately cool and well ven¬ 
tilated. Patients are rendered worse by being kept too hot. 
The occurrence of mania should be anticipated by careful 
watching and by having the windows barred. The diet 
should be of milk. 

The fever is best treated on hydropathic principles; the 
headache and backache are to be combated by opium or 
phenacetine. Sleep may be procured by sulphonal, chloral- 
amide, or codeia. 

The patient should, if possible, be prevented from scratch¬ 
ing. Great care should be exercised in the strictest cleans¬ 
ing of the eyes and in preventing them from being infected 
by their being rubbed with pus-stained hands. For the 
cleansing a saturated solution of boric acid is to be pre¬ 
ferred. 

As the extent of the pitting depends entirely upon the 
depth of the pustules, there is no method of treatment 
known by which pitting can be prevented. It seems, how¬ 
ever, that the intensity of the pustules is modified by ex¬ 
cluding the light and by keeping them covered with strips 
of gauze constantly wet with weak solutions of bichloride 
or of carbolic acid. This application also relieves the pain 
and itching. Isolated pustules may be painted twice a day 
with 10 per cent, carbolic acid in alcohol. When crusts 
form they are to be softened by applications of lard or of 
vaseline to prevent them from floating in the air and thus 
carrying the infection. The other symptoms and compli¬ 
cations should be treated on general principles. 


64 MANUAL OF THE PRACTICE OF MEDICINE. 


VACCINIA; VACCINATION. 

Vaccination was first performed in 1798 by Jenner, and 
its value is now universally acknowledged. The vaccine 
may be procured by means of the scabs of patients vacci¬ 
nated humanized virus), or be taken direct from the calf 
bovine virus). If the humanized virus be used, it is of the 
utmost importance that it be taken from a healthy subject 
free from even* trace of syphilitic and tubercular taint. As 
a rule, bovine virus obtained fresh from reliable sources 
should be used. 

In a primary vaccination there appears in from twenty- 
four to thirty-six hours a papule which on the fifth or sixth 
day becomes an umbilicated vesicle surrounded by an indu¬ 
rated inflammatory zone. This papule on the eighth or 
ninth day changes to a pustule, which dries up, and the 
brownish scab resulting falls off on the twentieth to the 
twenty-fifth day, leaving the characteristic scar. In patients 
who have already been vaccinated successfully there may 
be either no result, or an irregular atypical vesicle, or a local 
ulceration on an inflammatory base. 

About the third dav of vaccination there begins a moder- 
ate fever, often preceded by chilly feelings, with malaise, 
restlessness, and irritability, these symptoms being espe¬ 
cially marked in children. These symptoms increase mod¬ 
erates* until pustulation is completed ; then they subside. 
The neighboring lymphatic glands become swollen, painful, 
and tender. 

The protection afforded varies with the completeness of 
the vaccination and with the time that has elapsed since it 
was last performed. Even* baby should be vaccinated, 
preferably between the second and third months, and 
thereafter even* seven years—oftener, however, if exposed 
to small-pox or during an epidemic. Should, under these 


VARICELLA. 65 

latter circumstances, a revaccination be unsuccessful, it 
should be repeated. 

Complications of vaccination are due either to lack of 
cleanliness or to impure virus employed, and should not 
occur if proper precautions be taken. There may be slough¬ 
ing ulcers, gangrene of the skin, or erysipelas. Septicaemia 
may develop in neglected cases. Impetigo contagiosa has 
been known to result. The patient may be inoculated 
with syphilis from humanized virus taken from diseased 
patients, the double infection resulting in the primary lesion 
at the site of inoculation. There may be observed vesicles 
about the inoculation, or a general eruption of vesicles from 
absorption of the virus. 

VARICELLA. 

Definition and Synonym.—Varicella is a contagious dis¬ 
ease especially of childhood, and is characterized by a vesic¬ 
ular eruption. Synonym: Chicken-pox. 

Etiology.—Varicella occurs in sporadic, endemic, and epi¬ 
demic forms. It is contagious throughout its course, but 
the contagious principle is of a low grade of intensity. It is 
almost exclusively a disease of children, but it may occur 
in young adults. One attack does not afford absolute im¬ 
munity from subsequent attacks. 

The exact virus has not been determined definitely. 
There is no connection, immediate or remote, between this 
disease and variola or varioloid. 

Symptoms.—The period of incubation is from eight to 
seventeen days, and it is unattended by symptoms. The 
invasion is marked by chilly feelings in some patients and by 
feverishness, the temperature rarely being higher than 102° 
F. except in very young children, in whom a fever of 104° 
F. is not unusual Convulsions are rare at the onset. There 
is apt to be vomiting, and the child complains of lassitude 
5 


66 MANUAL OF THE PRACTICE OF MEDICINE. 


and of pains in the back and legs. These symptoms last 
for but a few days. In some cases the constitutional symp¬ 
toms are so slight that except for the eruption the child may 
seem well. 

The eruption appears in about twenty-four hours, first 
on the chest and back or on the forehead and face, and con¬ 
sists of small raised spots which in a few hours become 
vesicles. These vesicles vary greatly in size, the larger ones 
usually appearing on the forehead ; they are rarely umbili- 
cated ; they collapse, as a rule, by a single puncture ; they ap¬ 
pear superficial, and not deeply seated ; and they are but 
rarely surrounded by an inflammatory halo. A few vesicles 
become pustular, but the majority in a day or so simply shrivel 
up, leaving crusts which fall off, usually leaving no cicatrices, 
although circular scars may result from the larger and 
deeper vesicles. Fresh crops of eruption appear during the 
first two or three days, so that the eruption can be seen in 
all stages of development. The eruption also appears in 
any of the mucous membranes; the vesicles, becoming 
macerated, leave superficial ulcers. 

In a few cases there appears a scarlatinal rash before the 
regular eruption. In rare cases, in debilitated children, 
there may be gangrene of the skin, or hemorrhages into the 
eruption and skin and from mucous membranes. 

The prognosis is regularly good except for the severer 
forms in very puny, weakly children. 

Treatment.—The patient should be kept in bed during 
the febrile stage, and in the house until the skin is free and 
clear. A child should be isolated from other children, but 
may associate with adults. 

SCARLET FEVER. 

Definition and Synonym.—Scarlet fever is an acute in¬ 
fectious, contagious disease with an eruption, fever, and 


SCARLET FEVER. 67 

pharyngitis, and with a tendency to cause an inflammation 
of the kidneys. Synonym: Scarlatina. 

Etiology.—The disease is contagious from the invasion 
until the end of desquamation. The poison is conveyed by 
the exhalations of the patient, by personal contact, or through 
the medium of a third person, and is spread by the scales of 
the desquamation; these scales, which float in the air and are 
deposited in clothing, bedding, and rooms, may remain in the 
hair long after convalescence. The poison possesses extra¬ 
ordinary vitality, so that contaminated' fomites may convey 
the contagion even after months or years. The poison 
may be carried great distances and may be conveyed also 
in milk. The exact nature of the poison has not definitely 
been determined. 

The disease occurs both in isolated cases, due always to 
contagion of some previous case, and in epidemics, which 
vary greatly in their virulence. It is most common in the 
fall and winter months. 

Susceptibility to the disease varies, some people being 
exempt. This exemption may run in families. The 
disease usually attacks children, 50 per cent, of all cases 
occurring before the fifth year, 90 per cent, before the tenth 
year. Young infants are rarely attacked. Adults become 
less and less susceptible with advancing years. One attack, 
with but the rarest exception, procures future immunity. 

The disease is said to occur with special frequency in 
puerperal women and after surgical operations, but it is 
now supposed that these cases are really septicaemia with a 
septic erythema, which often desquamates, as does any long- 
continued hyperaemia of the skin. 

The relation between scarlet fever and diphtheria is at 
present unsettled. A patient may have the two diseases 
together from a mixed infection, or a scarlatina may occur 
with membrane in the throat, or a diphtheria may occur 


68 MANUAL OF THE PRACTICE OF MEDICINE. 


with a septic erythema. Careful bacterial investigations are 
required to settle the relationship of the two diseases. 

Pathology.—The characteristic lesions consist in the 
eruption and the pharyngitis. No traces of the eruption 
are observed after death, except in the hemorrhagic form. 
The pharynx usually presents the appearance of a catarrhal 
inflammation. 

The complicating inflammations are exceedingly numer¬ 
ous and important. There may be follicular tonsillitis or 
pseudo-membranous inflammation of the tonsils, pharynx, 
or larynx. There may be cellulitis of the neck that may 
go on to gangrene or suppuration, the pus containing strep¬ 
tococci. There may be infection of the middle ear with 
otitis media, perforation, and deafness. 

Respiratory complications are not common, although 
broncho-pneumonia may occur. In rare cases there may 
be pericarditis or endocarditis, and less frequently menin¬ 
gitis. The spleen is usually found enlarged during the 
height of the disease. 

In nearly all cases there is found a parenchymatous 
degeneration of the kidney, but there may be either acute 
exudative or acute diffuse nephritis. These renal changes 
are the most important and formidable of all the complica¬ 
tions of the disease, constituting the so-called “ scarlatinal 
nephritis.” 

Symptoms.— Incubation .—This period is pretty con¬ 
stantly seven days, although its extreme limits are between 
twenty-four hours and two weeks. During this period 
there are no symptoms. 

Invasion .—The invasion is sudden and striking, being 
marked by fever, sore throat, and vomiting. This trinity 
of symptoms occurring suddenly should always excite the 
suspicion of scarlatina. There may be initial chilly feelings, 
or convulsions in young children. An actual chill is rare. 


SCARLET EEVER. 


69 


The vomiting, which is usually severe and apparently 
uncalled for, may be projectile. The fever mounts rapidly, 
and reaches 103° to 105 0 F. within a few hours, few diseases 
showing such a rapid rise. There is pain on swallowing; 
the throat is dryish ; the glands at the angle of the jaw are 
swollen and tender. On inspection there may be only the 
appearance of a catarrhal pharyngitis either mild or severe, 
or there may be added a follicular tonsillitis. 1 he pulse 
becomes rapid and is usually of high tension. The face is 
flushed, and the child at once looks seriously ill. There may 
be repeated convulsions or talkative delirium, according to 
the severity of the disease and the nervous constitution of 
the patient. There is usually some nocturnal wandering of 
the mind. In rare cases either the vomiting, the fever, or 
the sore throat may be absent. 

Eruption .—The eruption appears on the evening of the first 
or on the second day, twelve or twenty-four hours after the 
onset, although it may be delayed until forty-eight hours; it 
consists of minute red points, not elevated above the level 
of the skin, appearing first on the throat, breast, and back, 
and rapidly spreading over the entire body, imparting to it 
the color of a boiled lobster. The chin and the mouth are 
usually left clear, giving a highly characteristic appearance 
and making diagnosis easy between this disease and measles 
or small-pox. The face, moreover, is not usually so much 
involved as in measles. By stroking the rash white lines 
stand out with characteristic vividness. The eruption may 
cover the entire body, or it may appear in patches sepa¬ 
rated by areas of normal skin, giving a peculiar mottled 
appearance, or in rare cases the eruption may appear only 
on the face, the body, or the extremities. 

There is usually considerable itching, especially during 
the intensity of the eruption. When the eruption is well 
marked the skin is often diffusely swollen and inflamed, pro- 


70 MANUAL OF THE PRACTICE OF MEDICINE. 

ducing an uncomfortable feeling of tension. The rash lasts 
for two or three days and then gradually fades. 

While the eruption is developing the pharyngeal symp¬ 
toms continue. After the initial vomiting of the onset there 
are rarely gastro-intestinal symptoms. The tongue presents 
the so-called “ strawberry ” appearance, the papillae in the 
tip and edges standing out like shining red pearls above the 
epithelial coating. The fever remains high during the 
development of the eruption, frequently reaching as high as 
105° or 106 0 F., and then gradually subsides with the fading 
of the eruption, becoming normal about the seventh day, 
although there is frequently a slight afternoon rise through¬ 
out the entire period of desquamation. At the height of the 
fever there are apt to be nervous symptoms—restlessness, 
nocturnal wanderings, or even delirium with convulsions— 
but with its subsidence these symptoms rapidly improve, 
the pharnygitis disappears, and convalescence begins. 

Desquamation .—Desquamation begins, after the fading 
of the eruption, in large flakes. This desquamation is espe¬ 
cially noticeable about the hands and feet, epidermal casts 
of the fingers and toes being frequently thrown off entire. 
These flakes are potent factors in the spread of the disease, 
and the patient should not return to ordinary life until 
desquamation is completed. Usually desquamation lasts 
into the third or fourth week, but it may last much longer. 
It is exceedingly rare for it to be absent altogether. 

Variations from the regular course of scarlatina are fre¬ 
quently observed, and are due in most part to varying inten¬ 
sity of infection. Of these variations, mention will be made 
only of the most common. 

1. Mild and Rudimentary Cases .—The invasion is marked 
only by a slight transitory fever and moderate angina. The 
eruption may be scanty, extending over a small portion 
of the body only, disappearing in from a few hours to a 


SCARLET FEVER. 


7 1 


day, or it may be absent altogether. There is usually, fol¬ 
lowing the eruption, a slight though evident desquama¬ 
tion lasting into the second or third week. These cases 
are frequently spoken of as “ sympathetic sore throats,” 
and are usually seen in partially unsusceptible adults 
who have been exposed to scarlatina. They are really 
true cases of mild scarlatina, and are not only capable 
of spreading the disease, but may also be followed by com¬ 
plications, especially nephritis. To such a rudimentary 
scarlatina many a supposedly primary nephritis owes its 
origin. 

2. Severe and Prolonged Cases .—The onset is usually severe, 
the temperature rising to io6° or 107° F. and the prostra¬ 
tion and cerebral symptoms being pronounced. The erup¬ 
tion in these cases may be scanty. The fever and the con¬ 
stitutional symptoms usually continue into the second week. 
These are bad cases, but they are not to be considered as 
hopeless. 

3. Malignant Cases .—The invasion is marked by a rapid 
rise of temperature, frequently as high as 106° or 108° F., 
with cerebral symptoms of ominous gravity—restlessness, 
delirium, convulsions, passing into coma. There is urgent 
dyspnoea; the pulse becomes increasingly rapid and feeble. 
In these cases the patient is overwhelmed by the virulence 
of the poison, and dies in coma or collapse in from eighteen 
to thirty-six hours. As a rule, there is no eruption, although 
a scanty atypical rash may appear should the patient live 
to the second or third day. 

4. Hemorrhagic Cases .—These are severe cases with a 
disposition to bleed from the mucous membranes and into 
the skin, the latter hemorrhages appearing as petechiae and 
large ecchymoses. Cerebral symptoms are apt to be pro¬ 
nounced. There are usually vomiting and diarrhoea, and 
frequently dyspnoea. The temperature may not be high. 


72 MANUAL OF THE PRACTICE OF MEDICINE. 


The prognosis is bad, the patient usually dying in two or 
three days. 

5. Angina Cases. —This type of scarlet fever is character¬ 
ized by the predominance of throat symptoms and compli¬ 
cating inflammations. The pharynx and fauces are usually 
intensely inflamed and their tissues much swollen, making 
speech and swallowing painful and difficult. There is fre¬ 
quently a membranous exudate which may spread from 
the pharynx and tonsils to involve the naso-pharynx and 
nose, or downward to the larynx, where the membrane may 
cause obstruction to the breathing and asphyxia. There 
may be necrosis of the throat-tissues that may lead to large 
sloughs, and if large arteries are involved fatal hemorrhage 
may result. The glands of the neck become enlarged, and 
frequently proceed to abscesses and cellulitis. Otitis media 
is apt to result by infection through the Eustachian canals. 
The patient rapidly passes into profound sepsis with its 
attendant symptoms—a condition which is rarely recovered 
from. 

Complications.— 1. Sufficient mention has already been 
made of the important throat and ear complications and of 
the glandular swelling and suppurations. 

2. The complicating lesions of the kidneys are exceedingly 
common. Very few cases of scarlatina run their course 
without the kidneys being involved in one of three ways : 
(1) by acute degeneration ; (2) by acute exudative nephritis ; 
(3) by acute diffuse nephritis. These varieties of nephritis 
have been admirably differentiated by Delafield, and his 
classification will be followed. 

(<?) Acute degeneration of the kidney , or parenchymatous 
nephritis, belongs to the first and second weeks of the dis¬ 
ease, and is not different from the degeneration occurring in 
the course of any severe infectious disease. The urine may 
be diminished slightly in quantity, and it usually contains 


SCARLET REFER. 


73 


albumin and casts in moderate amounts. The course is 
mild, unattended by constitutional symptoms, and ends in 
recovery. 

(f) Acute exudative nephritis belongs to the second and 
third weeks, following' either a mild or a severe attack of scar- 
latina. In severe cases the urine is scanty or suppressed ; 
its gravity usually is unchanged ; albumin and casts are 
abundant; there may be blood. There are uraemic symp¬ 
toms—headache, nausea and vomiting, dyspnoea, convulsive 
twitchings. In some cases there is added contraction of 
the arteries with high-tension pulse and disturbed heart- 
action. The patient becomes anaemic and the face puffy, 
the oedema frequently becoming general with fluid in the 
serous cavities. The temperature is raised, and it remains 
remittingly high during the acute stage of the nephritis. 
In mild cases there may be only moderate changes in 
the urine; uraemic symptoms may be unobserved. The 
fever is slight or absent. Between these two there are all 
grades of severity. These cases run about four weeks and 
usually terminate in recovery, a small proportion only being 
fatal. 

(c) Acute diffuse nephritis occurs in the third week and 
during convalescence. It is really a post-scarlatinal nephri¬ 
tis, and may develop after either mild or severe cases. It 
runs an acute or a subacute course. The acute cases begin 
suddenly and resemble a severe attack of exudative nephritis. 
The subacute cases develop gradually. There is apt to be 
repeated vomiting, which is always to be regarded with sus¬ 
picion in a patient convalescing from scarlatina. Anaemia 
and dropsy progress slowly. The urine is regularly dimin¬ 
ished in quantity, and it contains abundant albumin and 
casts. In some cases the primary changes are the first 
symptom. In all cases of diffuse nephritis the disease is apt 
to continue with more or less rapidity, with or without re- 


74 MANUAL GF THE PRACTICE OF MEDICINE. 

mission, until the death of the patient In rarer cases the 
lesion becomes chronic. 

3. Inflammation of serous membranes , meningitis, may 
occur. Endocarditis and pericarditis are more frequent. 
The so-called “ scarlatinal rheumatism ” occurs usually as 
the eruption is fading, and involves especially the hands and 
feet, although the large joints may be affected as well. The 
joints are painful, and may be swollen and inflamed. The 
process is septic, and not rheumatic, in its nature. Recovery 
is effected in a few weeks, though suppuration or permanent 
deformity may result. 

4. Inflammation of the muscles , myositis, may occur, espe¬ 
cially in the neck-muscles, with pain, tenderness, and con¬ 
traction. The muscles may in rare cases remain perma¬ 
nently contracted. 

The prognosis is influenced by the character of the epi¬ 
demic (5 to 30 per cent, mortality), the age and general con¬ 
dition of the child, the severity of the attack, and the nature 
of the complications. A guarded prognosis must always be 
given, as dangerous complications, especially nephritis, may 
occur even during convalescence. 

Treatment.—The patient should be isolated strictly until 
the completion of desquamation. The room should be well 
ventilated, free from draughts, and should have a tempera¬ 
ture of about yo° F. The patient should be kept in bed 
until the temperature has been normal for a week, after 
which time the child may be allowed about the room. The 
diet should be of milk during the febrile period ; broths, 
eggs, fruit, and light cereals may be allowed during early 
convalescence; but no animal food should be taken until 
the fourth week. The best preventive of nephritis is a rigor¬ 
ous milk diet. 

There is no specific medication. Symptoms must be 
treated on general principles. 


SCARLET FEVER. 


75 


Fever .—At the onset aconite may be given in drop doses 
every quarter of an hour until arterial tension is decreased, 
and then every two or three hours to hold the pulse at that 
point. Should the fever be high, it is best treated by hydro¬ 
therapy, which has the additional advantage of calming 
the nervous symptoms. For this purpose baths, the cold 
pack, sponging with water, or the ice-cap may be employed 
without the least danger. The “ driving in ” of the erup¬ 
tion, with disastrous consequences, is mythical. Internal 
antipyretics should not, as a rule, be employed. 

The nervous symptoms may be controlled by hydro¬ 
therapy, by phenacetine (gr. ij—v) to a child five years of 
age, or by chloral. The following prescription has been 
proven useful: 

IChloral hydrate, gr. ij; 

Camphor-water, TTtxv; 

Syrup of orange-peel, ad gj.—M. 

Sig. Dose for a child four years old, repeated every three 
or four hours. 

Or, fy. Chloral hydrate, gr. ij; 

Peppermint-water, 3 ss.—M. 

Sig. Dose for a child four years old, every three or four 
hours. 

This prescription is also valuable to correct the initial 
vomiting. 

The pharyngitis should always be treated. Gargles do 
not prove of much use in children, and rarely in adults. Po¬ 
tassium chlorate is to be avoided because of its toxic effects 
on the kidneys. The pain is best relieved by cloths wrung 
out of hot water, applied frequently to the neck and covered 
by oil silk. In some cases cold applications to the throat 
are more grateful. The mouth and throat must be kept clean 
to avoid the spread of the infection, they being frequently 


j6 MANUAL OF THE PRACTICE OF MEDICINE. 


rinsed out with a saturated solution of boric acid, and 
sprayed every two to four hours with a solution of bichlo¬ 
ride of mercury (i : 5000) or with peroxide of hydrogen 
(3 per cent, solution). 

The daily anointing of the skin with a bland antiseptic 
ointment relieves the itching and the feeling of tension and 
prevents the dissemination of the scales. Lard, cacao butter, 
or olive oil may be used, to each ounce of which carbolic 
acid (gr. xx), thymol (gr. x), or menthol (gr. x) may be 
added. Previous to the inunction the skin should be cleansed 
daily with soap and warm water. 

The temperature should be taken at times during con¬ 
valescence. The heart, lungs, and urine should be exam¬ 
ined every few days, even if the progress of the case seems 
satisfactory. 

Nephritis is to be treated as though it were a primary 
disease. 

The septic inflammation of the joints is best treated by 
hot applications and by saline laxatives. Ichthyol ointment 
(3ss to sj) may be serviceable. Salicylic acid and its deriva¬ 
tives occasionally seem to do good, but they are uncertain. 

Cervical adenitis and cellulitis are to be treated on gen¬ 
eral rules. 

Before the patient returns to ordinary life desquamation 
must be over entirely. Several warm cleansing baths with 
repeated shampooing are to be employed to remove all 
scales from the skin and the hair. 

MEASLES. 

Definition and Synonym.—Measles is an acute conta¬ 
gious disease characterized by an initial coryza and a maculo- 
papular eruption. Synonym: Rubeola. 

Etiology.—The disease is endemic, and from time to time 
assumes epidemic proportions. It most frequently attacks 


SCARLET FEVER.—MEASLES. Plate 



• Scarlet fever. 2 . Measles. 
























































































































































































i 

































































MEASLES. 


77 


children, especially those under eight years of age, but un¬ 
protected adults are more liable to the infection than to 
scarlet fever, the infection being more intense and suscepti¬ 
bility to it being much more universal. It is contagious 
throughout its course, especially during the eruption, and 
there are grounds for believing it contagious even during 
the period of incubation. The poison is conveyed by the 
breath, by the secretions, especially of the nose, and by 
the branny desquamation. It may be carried by the air, by 
fomites, or by a third person. One attack does not always 
procure immunity, but there may be a second, a third, or 
even a fourth attack, although recurrences are not so com¬ 
mon as supposed. 

The exact contagion has not been determined, but it is 
known to possess less vitality and a shorter duration of life 
than the poison of scarlet fever. Under ordinary circum¬ 
stances it is usually a mild disease, but epidemics in crowded 
tenement-houses and in armies may become serious, while 
epidemics occurring for the first time in savage tribes may 
be exceedingly fatal, the mortality being bven 25 per cent, 
of the entire population. 

Pathology. —The eruption and the catarrhal inflammations 
of the conjunctivae and the upper respiratory tract constitute 
the essential lesions. As complicating lesions there may 
be found broncho-pneumonia, capillary bronchitis, swelling 
of the bronchial glands, and less frequently pleurisy or lobar 
pneumonia. There may be hyperaemia of the gastrointes¬ 
tinal mucosa with swelling of Peyer’s glands. 

Symptoms.— The period of incubation is from ten to 
fourteen days, rarely so long as twenty days. During this 
time there are usually no symptoms, although in some cases 
the child may be feverish and irritable. 

Invasion .—The child becomes listless and exhibits the 
symptoms of a feverish cold. There are usually shivering 


78 MANUAL OF THE PRACTICE OF MEDICINE. 

attacks, but a regular chill or an initial convulsion is rare. 
There are redness of and running from the eyes, with pho¬ 
tophobia, sneezing, snuffling, and running from the nose, 
followed by cough and hoarseness. Sore throat is some¬ 
times complained of, but is not so common nor so severe as 
in scarlet fever. Examination may show hyperaemia with 
small red spots on the hard and the soft palate. The tem¬ 
perature rapidly rises to 102° or 104° F., remitting some¬ 
what on the second and third days, becoming again elevated 
upon the appearance of the eruption. There may be nausea 
or vomiting and nervous symptoms depending on the sever¬ 
ity of the attack and the constitution of the child. In some 
cases these symptoms are slight, the child not feeling well, 
having apparently a trifling cold with but moderate feverish¬ 
ness. The stage of invasion lasts for three or four days. 

The Stage of Eruption .—The eruption usually appears on 
the fourth day, being seen first on the face and neck, and 
then rapidly spreading over the chest and body. It consists 
of small round spots, slightly elevated, so that they may 
impart a shotty feeling to the finger; these spots increase 
in size and assume a roundish or crescentic outline. The 
rash is hyperaemic, disappearing on pressure, although in 
some cases there may be petechiae. The rapidity of develop¬ 
ment varies, the eruption becoming characteristic in some 
cases in a few hours, in other cases not for several days. 
The eruption closely resembles that of poisoning by shell¬ 
fish or that produced by antipyrine. The eruption is fully 
developed by the end of two or three days, and then begins 
to fade, being followed by a fine branny desquamation. At 
the height of the eruption there may be some swelling and 
inflammation of the intervening skin, but usually it is nor¬ 
mal in appearance. 

When the eruption appears the temperature again rises, 
reaching its maximum at the time of the greatest development 


MEASLES. 


79 


of the eruption, after which, usually in the second day of the 
eruption, the temperature begins to fall, frequently by crisis. 
Restlessness, sleeplessness, or even general convulsions and 
delirium, may accompany the exacerbation of the fever. 
The catarrhal symptoms attain their maximum while the 
eruption is developing, and then gradually subside. 

Variations in its Course.—i. In rare cases there may be 
no catarrhal symptoms during the period of invasion. 

2. There are very light cases in which there may be no 
eruption. After the regular period of incubation the patient 
becomes indisposed, feverish, and has a coryza—as it is said, 
“ sickens for the disease,” but the eruption is not developed. 

3. In some cases the eruption appears as early as thirty- 
six hours, or it may be deferred until the sixth day. 

4. There are cases of marked severity characterized by 
high fever (105° or 106° F.) and cerebral symptoms, con¬ 
vulsions, delirium, and stupor. 

5. In some epidemics, especially in armies and in savage 
tribes where measles appears for the first time, may ap¬ 
pear malignant cases, the so-called “ hemorrhagic ” or 
“black” measles. The invasion is sudden and intense; 
prostration is extreme; there are convulsions or delirium 
or even coma. The eruption becomes hemorrhagic ; hem¬ 
orrhages occur in the skin and from mucous membranes, 
These cases are almost always fatal. 

Complications and Sequelae. —The most important are 
those of the respiratory system. A mild form of bronchitis 
is common to the disease, but in debilitated subjects, in 
asylum children, and in severe forms of the disease the in¬ 
flammation is apt to extend and to lead to broncho-pneu¬ 
monia. This complication runs a regular course, and is the 
cause of death in the vast majority of fatal eases. There may 
be a swelling of the bronchial glands that render them liable 
to tubercular infections, which may be the origin of acute 


So MANUAL OF THE PRACTICE OF MEDICINE. 


miliary tuberculosis. Thus in asylums fatal cases of tuber¬ 
culosis frequently follow epidemics of measles after a little 
interval. In some cases there may be a tubercular bron¬ 
cho-pneumonia at the start from added tubercular infec¬ 
tion. Lobar pneumonia and pleurisy may less commonly 
occur. There may be protracted and severe conjunctivitis. 
Croupous laryngitis may occur. There may be otitis 
media. 

In weakly children there occurs rarely gangrene of the 
cheeks or of the vulva (cancrum oris or noma). In some 
cases there is exhausting diarrhoea, which may assume a 
dysenteric character with bloody, slimy passages. True 
nephritis is rare, although albuminuria is common in the 
height of the disease. The disease may be complicated by 
whooping-cough. 

Prognosis. —The prognosis is generally good except 
when severe epidemics occur in tenements, armies, and 
among savage races in virgin soil. Death seldom occurs 
from the disease itself, but from pulmonary complications. 
The prognosis is not good in children under the age of two 
years. The possibility of subsequent tuberculosis must be 
considered. 

Treatment.—The patient should be isolated until desqua¬ 
mation is completed. Especial care should be exercised to 
to prevent delicate children with weak lungs or a tubercu¬ 
lar predisposition from being exposed to the disease. The 
room should be of an even temperature (about 70° F.) and 
well ventilated. There is no advantage in keeping the room 
too hot. The patient should remain in bed until three or 
four days after the fever has gone, and during the febrile 
period should be kept on a milk diet. Water may be given 
freely. The majority of uncomplicated cases need no further 
treatment, though special symptoms may be treated as they 
arise. 


RUBELLA. 


8 I 


The fever rarely needs treatment. Should it be high 
(over 104° F.) f it may be reduced by sponging with water. 
Cool baths may be employed with benefit. 

Conjunctivitis is best treated by careful cleansing of the 
eyes with a saturated boric-acid solution; or a few drops 
of a solution of atropia (gr. j : 3j) or of alumnol (gr. v : 3j) 
may be employed. For the redness of the eyelids the un- 
guentum hydrargyri oxidi flavi (U. S. P.) may be used. In 
severe cases the room may be darkened slightly by blinds 
or by screens to relieve the photophobia. 

Restlessness, delirium, and sleeplessness are best con¬ 
trolled by sodium bromide or phenacetine. 

The cough, if troublesome, is best treated by paregoric 
and syrup of ipecac in small doses. 

The itching of the skin may be relieved by washing with 
a solution of bicarbonate of soda or by oiling the skin with 
lard or with cacao butter. 

Other symptoms as they arise are to be treated on 
general principles. During desquamation the skin should 
be oiled daily to prevent dissemination of the branny 
scales. 

During convalescence great care should be taken to build 
the child up and to avoid most especially the least possi¬ 
bility of tubercular infection. Too much care cannot be 
taken in this regard. 


RUBELLA. 

Etiology and Synonyms. —Rubella is rather rare, occur¬ 
ring chiefly as epidemics, which are frequently extensive. 
Sporadic and endemic cases are exceedingly infrequent. It 
is a disease entirely distinct from measles, although closely 
resembling it in many of its clinical features. It is conta¬ 
gious to both adults and children, and one attack procures 
6 


82 


MANUAL OF THE PRACTICE OF MEDICINE. 


future immunity. Synonyms: German measles; Roseola; 
Rotheln. 

Symptoms.— Incubation .—The period of incubation is 
usually two weeks. 

Invasion .—The symptoms of the invasion resemble those 
of measles, but are much milder and are of shorter duration. 
There is a slight fever, rarely over ioo° F., with headache, 
nausea and vomiting, coryza, sore throat, and swelling of 
the glands at the back of the neck that is almost charac- 
teristic. These symptoms rarely continue longer than 
twenty-four hours. In many cases they are so slight as 
to be unnoticed. 

The eruption , which appears in from twenty-four to forty- 
eight hours, is first seen on the face and chest, thence spread¬ 
ing generally. It consists of small round, raised spots, of a 
pinkish rose-color, which are usually discrete and which 
frequently are seen on the palate. They are rarely crescentic. 
They may become confluent, the consequent reddening 
of the skin closely resembling the scarlatina rash ; but the 
eruption is more erythematous, is not punctiform, and in 
places shows a papular character. In a certain number of 
cases there are developed from the papules a few vesicles 
which may become pustules. This is never the case with 
scarlatina nor with measles. 

The eruption lasts for two or three days and then fades. 
There may be a slight branny desquamation. 

During the eruption there may be some feverishness, an 
aggravation of the pharyngitis, and swelling of the glands at 
the back of the neck. In many cases, however, the only 
symptom is the eruption. 

The prognosis is perfectly good. 

Treatment.—Few diseases need so little treatment as 
rubella. The case should be isolated to avoid the spread 
of the disease. 


EPIDEMIC PAR O TIPIS. 


83 


EPIDEMIC PAROTITIS. 

Definition and Synonym.—Epidemic parotitis is an 
acute contagious disease characterized by inflammation of 
the salivary glands. Synonym: Mumps. 

Etiology.—Parotitis occurs both as an endemic and 
an epidemic disease, epidemics being usually extensive. 
It is a disease of childhood and adolescence, attacking - in- 
fants and elderly people but rarely. It is more frequent 
among males than among females. It is personally con¬ 
tagious from the last few days of the period of incubation 
until the subsidence of the symptoms. The exact poison 
has not been absolutely proven, although a bacillus paro- 
tidis has been described. 

Lesion.—The lesion consists in the swelling and conges¬ 
tion of one or of both parotid glands, and occasionally of 
the submaxillary glands as well. 

Symptoms.—The period of incubation is between two 
and three weeks and is unattended by symptoms. The 
disease begins with fever—usually not over ioi° F., 
but it may be as high as 103° or 104° F.—and at¬ 
tendant febrile symptoms, nausea, restlessness, and pros¬ 
tration. The local symptoms become noticeable in from 
twenty-four to thirty-six hours, although in some cases 
they may precede the fever. The patient complains of a 
feeling of tension, more rarely of actual pain with tender¬ 
ness, referred to the parotid gland of one side. The gland 
is swollen, giving the patient a characteristically comical 
appearance. Deglutition and speaking aggravate the pain. 
There may be pharyngitis or earache. 

The inflammation reaches its height in from three to six 
days and then subsides. It is usual for the inflammation 
to start on one side, the other parotid gland becoming 
affected in a day or so. More rarely both glands may be 


84 MANUAL OF THE PRACTICE OF MEDICINE . 

affected simultaneously, or the inflammation may be sub¬ 
siding on the side first affected before the involvement of 
the other side, so that the duration of the disease is doubled. 
The lesion is rarely unilateral throughout. 

In some cases the submaxillary glands may secondarily be 
involved. With the subsidence of the inflammation the fever 
and the constitutional symptoms disappear. 

While the course is generally mild, there are cases which 
run a severe course, with high fever, rapid and feeble heart- 
action, and delirium. 

Orchitis occurs more frequently in some epidemics than 
in others. It is rarely seen before puberty, and double 
orchitis is infrequent. The orchitis gives rise to pain and 
tenderness; the testicle is hard and swollen ; there may be 
fluid in the tunica vaginalis. 

The temperature rises, frequently to 103° or 104° F., and 
remains high until the orchitis begins to subside, which is 
usually in from five to ten days. Subsequent involvement 
of the other testicle may prolong the disease for another 
week. In females there may be vulvo-vaginitis, or the 
breasts may be enlarged and tender. Inflammation of the 
ovaries is rare. 

Complications and Sequelae. —There may be meningitis, 
mania, or post-febrile insanity. There may be suppuration 
or gangrene of the parotid glands. Severe orchitis may be 
followed by atrophy. In some cases arthritis has been ob¬ 
served. There may be deafness, which frequently is per¬ 
manent. 

Treatment. —The patient should be isolated until the dis¬ 
appearance of acute symptoms, and during the febrile period 
should be kept in bed and on a light diet. The parotiditis 
is best treated locally by applications of cold ; should, how¬ 
ever, heat be more grateful, poultices, applications of hot 
cloths, or dry cotton covered with oiled silk may be em- 


WHOOPING-COUGH. 85 

plo} ed. Resolution may be hastened by applications of 
ichthyol ointment (3ss : sj) or of iodine ointment. 

Orchitis is to be treated by rest in bed, elevation of the 
testicle, and applications of cold. " In the latter stages ich¬ 
thyol ointment or unguentum plumbi iodidi may be em¬ 
ployed with benefit. Other symptoms should be treated on 
general principles. 

WHOOPING-COUGH. 

Definition and Synonym. —Whooping-cough is an acute 
contagious disease with inflammation of the respiratory tract, 
a paroxysmal cough, and a characteristic “ whoop.” Syn¬ 
onym: Pertussis. 

Etiology. —Whooping-cough occurs in endemic and epi¬ 
demic cases, the epidemics being most frequent in the winter 
and early spring months, and often being associated with 
epidemics of measles. The disease is personally contagious, 
though concentrated and prolonged exposure is usually 
required. One attack procures immunity. The actual 
cause is probably due to a short bacillus growing in cultures 
with well-marked characteristics, first described in 1887 by 
Afanassjew. The majority of cases occur in children under 
six years of age, though no age is exempt. In negroes it 
runs a more severe course. 

Lesion. —The lesion consists in a catarrhal inflammation 
of the nose, larynx, trachea, and bronchi. As complicating 
lesions there may be found extensive bronchitis of the smaller 
tubes, broncho-pneumonia, inflammation of the bronchial 
glands, and emphysema of the vesicular or interlobular 
variety. 

Symptoms. —The incubation period of the disease is about 
two weeks, although this is difficult to determine owing to 
the insidious onset. The symptoms begin with bronchitis 
and coryza similar to those of an ordinary severe cold; these 


86 MANUAL OF THE PRACTICE OF MEDICINE. 

symptoms continue without improvement for from one to 
three weeks. Then appear the characteristic coughing 
attacks from which the disease is named. The attack be¬ 
gins with a series (fifteen to twenty) of coughs so rapid and 
spasmodic that the child cannot breathe. Suffocation seems 
imminent; the face is suffused; the eyes run; the tongue 
is cyanotic and protruding. The child is terrified and sits 
up in bed or runs to the nurse or the mother. After this 
series of coughs there is a long, deep inspiration with the 
sound of the characteristic whoop, immediately after which 
the convulsive coughs may be repeated. In some cases the 
whoop is the first indication of a coughing attack. In rare 
cases there is only the paroxysmal cough without any 
whoop. The attack is often followed by the raising of a 
little tenacious mucus, which gives relief. 

Very severe attacks may be accompanied by vomiting or 
regurgitation of food, by relaxation of the sphincters, by 
convulsions, or by hemorrhages from the nose, mouth, 
stomach, or under the conjunctiva. In rare cases there 
may be symptoms of cerebral or subdural hemorrhage. 
The number of separate attacks varies from three to eighty 
during the twenty-four hours. The attacks are frequently 
induced by emotions, by crying, by attempts at swallowing, 
by close, dusty air, and by changes in temperature, and they 
are usually more frequent at night than during the day-time. 

The general health suffers. Severe cases are accompanied 
by fever and prostration. The vomiting and the induce¬ 
ment of an attack by swallowing interfere with proper nutri¬ 
tion, while the child is nervous and fretful from loss of 
sleep. There is usually found superficial ulceration on each 
side of the frenum of the tongue, and between the attacks 
the face is frequently swollen, the lower lids are puffy, and 
the tongue is enlarged and of a bluish color. 

After the paroxysmal stage has lasted for from three to 


WHO OPING- CO UGH. 


37 


six weeks the attacks become less severe, the whoop ceases, 

and there remains only a terminal bronchitis which slowly 

declines. The whole duration of the disease is in this way 

protracted for from six to twelve weeks. In adults the 

disease runs a more severe and energetic course, with 

<=> ’ 

marked depreciation in general health. 

Complications and Sequelse.—The pulmonary complica¬ 
tions have been mentioned under the heading of Lesions. 
Their association with whooping-cough renders the prog¬ 
nosis much worse than if they occurred primarily. 

Paralysis from cerebral or intradural hemorrhage is a rare 
sequela. 

Whooping-cough is frequently followed by acute tuber¬ 
culosis or by tubercular broncho-pneumonia, from an added 
infection of the inflamed lung or the bronchial glands. Qui¬ 
escent tubercular deposits may also be called into activity. 

In some cases there will be a return of the whoop at inter¬ 
vals for months whenever bronchitis is contracted. This is 
not a recurrence, but is merely a “ habit-spasm.” 

Treatment.—Every possible care should be employed to 
keep children, especially if delicate, from being exposed. 
Negligence in this regard is criminal. The contagion is 
most marked during the paroxysmal stage, and declines with 
the terminal bronchitis, but does not persist after the second 
month. Isolation and quarantine cannot be insisted upon 
to their full limits, and a final disinfection of the rooms and 
the clothing is not necessary, as the contagion is conveyed 
by the breath alone. The room should be sunny and well 
ventilated. In mild cases without pulmonary complications 
the child can go out in favorable weather. The proper 
feeding of the child is important, especially if there be 
vomiting during the attacks. 

Drug treatment is largely employed, and many alleged 
“ specifics ” are lauded from time to time. No one form of 


88 MANUAL OF THE PRACTICE OF MEDICINE. 


treatment is of service in all cases, but one drug after another 
has to be tried. 

During the catarrhal stage the treatment is that of the 
bronchitis. During the paroxysmal stage treatment is 
directed not only toward the bronchitis, but also toward 
the mitigation of the paroxysms. For the latter purpose 
internal sedatives and local applications are employed. 

Internal Sedatives .—The doses given are those suitable 
for a child two years old. 

Belladonna , frequently to tolerance. Initial dose, 2 min¬ 
ims of tincture every three hours. 

Quinine , in full doses, gr. j every two hours. 

Chloral , gr. ij-iv every four hours : efficient in many cases, 
especially to secure sleep ; may advantageously be combined 
with sodium bromide (gr. iij-v), especially in children with 
convulsive tendencies. 

Opium or codeia is to be used only in the severest cases. 

Asafcetida mixture is often of service in mild cases. 

Antipyrine (gr. i-iij every two or three hours) is often 
attended by most brilliant results. 

Phenacetine (gr. ij-iij every three hours) has been found 
useful. 

Bromoform (3 drops in simple elixir three times a day) 
acts almost as a specific in some cases. 

The disinfection of the sleeping-room with sulphur, the 
child sleeping there in clean clothes after the room has been 
aired, often cuts short the paroxysmal stage. 

Local treatment may be employed if not resisted by the 
child—inhalation of the vapor of carbolic acid, of creosote, 
atomized sprays of wine of ipecac, 1 per cent, solutions of 
resorcin, peroxide of hydrogen, or solutions of quinine. 

Insufflations of quinine, I per cent, solutions of resorcin, 
or a powder of salicylic acid gr. x. to boric acid 5ij, may be 
tried. 


EPIDEMIC INFLUENZA. 


89 


In many cases, during the decline of the paroxysmal stage 
a change of climate may hasten recovery. In severe and 
protracted cases it should always be tried. 

EPIDEMIC INFLUENZA. 

Definition and Synonym. —Epidemic influenza is an 
acute infectious disease, occurring principally in pandemics, 
characterized by fever, pains, prostration, and by inflamma¬ 
tion of the mucous membranes. Synonym : La Grippe. 

Etiology. —The disease occurs in epidemics which spread 
over whole countries or quarters of the globe with great 
rapidity, attacking large numbers of people. The epidemics 
usually start in the East, the majority arising in Russia. 
Until 1870, ninety such epidemics had been described. The 
last pandemic occurred in 1889-90. The disease is not 
affected by sex, age, condition of life, climate, or atmospheric 
changes. Sporadic cases occur in the wake of the epidemics. 
One attack does not procure immunity. The disease is 
probably slightly contagious by personal contact, and possi¬ 
bly through fomites, but in the large epidemics infection 
cannot be traced with any certainty. 

The actual cause of the disease appears to be a bacillus 
first described in 1892 by Pfeiffer. This is a short bacillus 
with bulbous ends that is found in the sputum, in the 
tissue of the lungs, and in the blood. This bacillus is never 
found in other diseases, is constant in grippe, and it causes 
the disease in monkeys and apes by inoculation. 

Lesions. —The regular lesion is a catarrhal inflammation 
of the respiratory passages, from the nose to the bronchi; 
frequently there are also swelling and hyperaemia of the 
mucosa of the stomach and intestines. 

Complicating lesions are numerous. The most import¬ 
ant are those of the respiratory organs. There may be lobar 
pneumonia, broncho-pneumonia, pleurisy, or empyema. 


QO MANUAL OF THE PRACTICE OF MEDICINE. 

Less frequently are noted abscess of the lung, abscess of 
the brain, meningitis, purulent pericarditis, and nephritis. 

Symptoms.—The symptoms are exceedingly varied, de¬ 
pending on the severity of the infection, the reaction on the 
nervous centres, and the varying intensity of the catarrhal 
inflammations of the respiratory and gastro-intestinal tracts. 
Complicating lesions also add their symptoms. 

1. Symptoms of Infection. —The onset is usually abrupt, 
being initiated by a chill or by chilly feelings. In some 
cases the chill is absent. Rarely there are prodromata, as 
evinced by lassitude of body and mind for several days. 
The temperature rapidly rises to ioi° to 104° F. accord¬ 
ing to the severity of the attack. There is marked prostra¬ 
tion from the first. The pulse is rapid and full. It may 
become feeble and intermittent, especially in the old and 
the debilitated, and may lead to heart failure. The liver and 
spleen in some cases are enlarged. 

2. Nervous Symptoms. —At the onset there is severe, 
agonizing headache, usually frontal, less frequently general 
or occipital. This headache is often as severe as in men¬ 
ingitis, persisting for hours or days, and it may be obsti¬ 
nately present during convalescence. 

Pain and tenderness of the muscles of the body, especially 
of the legs and the back, are constant symptoms. The 
patients feel bruised, and shift their position, trying to find 
one more endurable. 

There are great depression of spirits and an inability to 
concentrate the mind which may last long into convalescence. 
In severe cases there may be delirium of an active type with 
hallucinations. There may be herpes labialis or urticaria. 

3. Catarrhal Symptoms. —There are conjunctivitis, redness 
and oedema of the lids, and increased lacrymaticn. Coryza 
appears, with snuffling and sneezing. Laryngitis is attended 
by hoarseness, pain, and a severe paroxysmal cough which 


EPIDEMIC INFL UENZA. 


9 1 


often continues for weeks after the attack without being im¬ 
proved materially by medication. Pharyngitis and tonsil¬ 
litis are usually present. The bronchitis may be mild or 
severe, and is marked by harassing cough, muco-purulent 
sputa, which may contain blood, pain in the chest, and the 
ordinary physical signs. 

4. Gastro-intestinal symptoms consist in a heavily-coated 
tongue, persistent vomiting, diarrhoea, tympanites, and pain 
and tenderness over the abdomen. 

Course of the Disease. —The relative predominance of 
the above symptoms varies in different people and in differ¬ 
ent epidemics. In all cases the symptoms of general infec¬ 
tion are present, but the nervous, catarrhal, or gastro-intes¬ 
tinal symptoms vary so much in their relative intensity as 
to present three principal types of the disease—a nervous 
form, a catarrhal form, and a gastro-intestinal form. No 
strict line of demarcation between these different types can 
be made. 

Complications and Sequelae. —Pneumonia is by far the 
most frequent and fatal complication. There may be either 
broncho-pneumonia, especially in children, or lobar pneu¬ 
monia. The latter, which involves one or more lobes, with 
complete or incomplete consolidation, and which is always 
associated with an intense general bronchitis, differs from 
the ordinary course of lobar pneumonia in the following 
particulars : The onset may not be so abrupt, being insidious 
and of slow development. The expectoration is that of 
bronchitis, rusty sputum being usually absent. The bron¬ 
chitis is a marked feature, adding its symptoms and physi¬ 
cal signs. The temperature is lower than that of a primary 
pneumonia, and is frequently remittent. Cyanosis and heart 
failure are more frequent. The duration is longer and reso¬ 
lution is more tardy. The temperature falls gradually, as a 
rule, and not by crisis, and frequently persists after resolu- 


92 MANUAL OF THE PRACTICE OF MEDICINE. 

tion. The pneumonia is often “ wandering,” creeping from 
place to place until a considerable part of the lung has 
become involved. Empyema, pleurisy, abscess of the lung, 
meningitis, purulent pericarditis, and acute nephritis may 
occur during or after the attack, and give their regular 
symptoms. 

Convalescence is usually slow and tedious, and is at¬ 
tended often by weakness of body and of mind. There may 
remain obstinate insomnia or cough. Facial neuralgia or 
headache may persist, and in some cases is due to compli¬ 
cating empyema of the antrum of Highmore. There may 
be post-grippal insanity or peripheral neuritis. Deafness 
may result from otitis media. 

During and after epidemics of grippe the mortality from 
tuberculosis is manifestly increased, quiescent and chronic 
tubercular processes being stirred into activity. 

The duration of an uncomplicated attack varies between 
three and seven days. It may be protracted by reason of 
the complications. Convalescence may be either rapid or 
slow and tedious. 

Prognosis. —Grippe itself is rarely fatal except in elderly 
or debilitated people or in those suffering from advanced 
pulmonary, nephritic, or cardiac disease. In these cases 
the disease may terminate fatally from weakness or from 
cardiac failure. The prognosis is largely influenced by the 
nature and severity of the complications. 

Treatment, —It certainly seems that the severity of the 
attack can be modified by the administration of large doses 
of quinine at the onset. At least gr. xx-xxx should be 
given within the first twenty-four hours, cinchonism being 
controlled by phenacetine or by sodium bromide. Aside 
from this the treatment is entirely symptomatic. 

The headache and the pains in the bones and muscles are 
best relieved by repeated small doses of phenacetine, prefer- 


EPIDEMIC INFLUENZA. 


93 


ably combined with salol (each 5 grains every two hours). 
Antipyrine and antifebrine are to be avoided if possible, be¬ 
cause of their depressing effect. Bromides may be useful 
in controlling restlessness, and a hot bath followed by a 
1 o-grain dose of Dover’s powder is often of great comfort. 
Morphine or codeine may be employed in severe cases. 
If headache depends upon congestion of the frontal sinuses, 
inhalations of steam, creosote, or menthol are of service. 
The following prescription is most satisfactory for the 
purpose : 

II. Menthol, gr. x; 

Tinct. benzoin, comp., Zj. —M. 

Sig. A teaspoonful gradually added to a pitcherful of boil¬ 
ing water, to be inhaled three times a day. 

Sleep is best procured by sulphonal, chloralamide, or 
codeia. 

The vomiting is to be treated by regulating the feedings, 
by bismuth, or by morphine. 

Diarrhoea is to be checked by opium combined with 
astringents. 

The bronchitis is to be treated after the ordinary methods 
—by sedatives, by expectorants, and by counter-irritation 
applied to the chest. 

Pneumonia requires its appropriate treatment, especial 
care being taken to avert heart failure by the timely admin¬ 
istration of stimulants ; alcohol, digitalis, and strychnine are 
most usually employed for this purpose. 

The depressing and enfeebling influence of the disease 
during convalescence requires most careful attention. The 
patient should not return too soon to business; the diet 
should be supporting; all depressing influences should be 
avoided; and appropriate tonics should be administered. 
A change of air is often required. This supporting treat- 


94 MANUAL OF THE PRACTICE OF MEDICINE. 


ment is especially indicated in those who present evidences 
of tubercular disease. 


DENGUE. 

Definition and Synonyms.—Dengue is an infectious epi¬ 
demic disease of warm latitudes, characterized by febrile 
paroxysms, pain in the muscles and bones, and anomalous 
eruptions. Synonyms: Dandy fever; Breakbone fever. 

Etiology.—The disease appears in extensive epidemics 
confined to the tropics and the sub-tropics. It has occurred 
in the Southern United States. Large numbers of people 
are attacked, susceptibility being almost universal. One 
attack does not secure immunity. The disease is supposed 
to be contagious by personal contact and through fomites. 
Epidemics occur in the summer months, and are checked 
by colder weather. The exact poison has not been deter¬ 
mined. 

Pathology.—But little is known about the disease, as 
fatal cases are rare. There appear to be no essential lesions. 

Symptoms.—The period of incubation is about four days. 
The onset is abrupt, beginning with a chill or chilly feel¬ 
ings, or with convulsions in children. The temperature 
rapidly rises to 102° to io6° F. according to the severity 
of the attack, and is accompanied by ordinary febrile symp¬ 
toms. Cerebral symptoms are frequent in the cases with 
high temperature. At the onset are developed agonizing 
headache and backache. The muscles are sore and tender. 
The joints become painful, tender, and frequently red and 
swollen. The large and the small joints are equally affected. 
Prostration and depression are marked. In some cases there 
may appear a transitory erythematous rash. In rare cases 
there may be severe vomiting and purging. There may be 
hemorrhages from any of the mucous membranes in severe 
cases. Lymphatic enlargements are not uncommon. The 


EPIDEMIC CEREBRO SPINAL MENINGITIS . 


95 


febrile paroxysm lasts from three to five days and terminates 
by crisis, the fall of temperature frequently reaching the sub¬ 
normal, although in most cases a moderate fever remains. 
At the crisis there may be sweating or diarrhoea. As the 
fever falls the general symptoms disappear, the patient feel¬ 
ing better, though often prostrated and sore. 

The period of remission lasts from two to five days, and 
during it may appear a variety of eruptions which are not 
distinctive. There may be urticaria, erythematous eruptions 
of all kinds, or herpes. The severer forms may be followed 
by desquamation. 

After the period of remission there occurs a second par¬ 
oxysm of fever with a return of all the previous symptoms. 
This paroxysm, however, is mild and lasts only for two or 
three days, terminating again by crisis, after which conva¬ 
lescence is established. 

Convalescence is usually slow and tedious from mental 
and physical incapacity. 

The prognosis is almost uniformly favorable. 

Treatment. —There being no specific treatment, the 
symptoms must be treated on general principles. 

EPIDEMIC CEREBRO-SPINAL MENINGITIS. 

Definition and Synonym. —Epidemic cerebro-spinal men¬ 
ingitis is an acute infectious disease characterized by inflam¬ 
mation of the cerebral and spinal meninges. Synonym: 
Cerebro-spinal fever. 

Etiology. —This disease, which has been recognized only 
since the early part of the present century, occurs chiefly 
in epidemics, although sporadic cases are frequently seen. 
The epidemics are most frequent and severe in the cold 
winter months, and are favored by poor hygiene and by the 
crowding together of people, as in garrisons and barracks. 
Children are more susceptible than adults. There is no 


96 MANUAL OF THE PRACTICE OF MEDICINE. 

evidence that the disease may be transmitted by food or by 
drinking-water. The disease is not considered contagious 
by either personal contact or through fomites, although rare 
cases have been reported which render it imprudent to make 
too dogmatic an assertion in this regard. 

In almost all the recently-studied cases there is found in 
the exudate a lance-shaped coccus which appears identical 
with the diplococcus of pneumonia, and it appears most 
likely that this is the specific micro-organism of the dis¬ 
ease. It is frequently found associated with the ordinary 
pus organisms. 

Pathology.—The brain is usually congested. 1 he veins 
and sinuses are engorged with blood. The pia mater is infil¬ 
trated with an exudate of fibrin, serum, and pus to a greater 
or lesser degree. The infiltration may be confined to the 
base or it may be more generally distributed. It is more 
abundant along the course of the blood-vessels and in the 
sulci. The lateral ventricles are filled with serum, which 
may be turbid from admixture of pus. In children, as a 
rule, and occasionally in adults, this fluid may distend and 
dilate the ventricles, and in chronic cases after the meningitis 
has subsided the distention of the ventricles may continue 
as a chronic hydrocephalus. 

The pia mater covering the spinal cord shows similar 
inflammatory changes, especially on the posterior aspect. 
The brain-cortex is often infiltrated with pus, which may 
form small abscesses. The cerebro-spinal fluid, which is 
usually increased, may be turbid. In the exudate the lance¬ 
shaped cocci are found frequently with ordinary pus cocci. 
The lesions may involve the sheaths of the cranial nerves, 
leading to neuritis and perineuritis. In very malignant 
cases there may be no time for the lesion to develop before 
death. 

In rare cases the meningitis is of the cellular variety. The 


EPIDEMIC CEREBROSPINAL MENINGITIS. 97 

pia may appear normal or lustreless or congested. There 
is neither fibrin, serum, nor pus, but there is a marked pro¬ 
liferation of the connective-tissue cells of the pia. These 
cases usually run a different clinical course. 

The remaining lesions are not distinctive, being those 
common to all severe infectious diseases. There may be 
hemorrhages in the skin, in the serous membranes, and into 
the viscera. There is granular and fatty degeneration of the 
liver- and kidney-cells and of the heart-muscle. The spleen 
is usually enlarged and soft. 

Symptoms.—The period of incubation is usually short, 
varying from a few hours to several days. During this 
time the patients may complain of headache, slight feverish¬ 
ness, and lassitude. 

The onset is usually abrupt, being marked by a chill, 
fever, headache, and vomiting. The fever may reach to 
102° or 104° F., and does not run any typical course. 
While high fever belongs to the severe cases, the reverse 

o 0 

is not always true. In some cases the fever may not be 
marked. 

The headache is usually frontal, but it may be parietal, 
occipital, or general. It is a severe headache, persisting 
during sleep and periods of stupor, as evinced by moaning, 
clasping the head with the hands, or by the facial aspects 
of pain. There may be general pains in the bones and 
muscles. 

The vomiting is frequently severe and distressing, and 
does not depend upon the giving of tood or of drink. It 
may assume a projectile character. 

During the earlier stages of the disease there are nervous 
symptoms of irritation. The headache has already been 
mentioned. There are frequently psychical disturbances, as 
shown by delirium, which may be maniacal. Some patients 
show morbid erotic desires. There may be from time to 


7 


98 MANUAL OF THE PRACTICE OF MEDICINE. 

time a sudden sharp cry, the so-called “ hydrocephalic cry.” 
The functions of the cranial nerves are exalted. There are 
photophobia, usually with some amount of conjunctivitis, 
intolerance to sounds, facial neuralgia, and muscular 
twitching. 

The irritation of the spinal nerves is shown by pain, ten¬ 
derness, and contraction of the muscles of the back of the 
neck that may amount to opisthotonos if the muscles of the 
trunk are similarly involved. 

The skin is hyperaesthetic, the least touch causing exqui¬ 
site pain. General exaggerated reflexes are highly charac¬ 
teristic. There are twitchings and spasms, and frequently 
automatic movements of the muscles of the arms or legs. 
The attitude is one of flexion. 

The pulse is at first increased in proportion to the fever, 
becoming slowed and full when the brain begins to be com¬ 
pressed by the effusion and distention of the ventricles. It is 
often remarkably variable in its rapidity. 

Various atypical eruptions may be seen on the skin. 
Herpes on the lips or the face occurs in half the cases. As 
the herpetic vesicles frequently contain the characteristic 
micrococci of the disease, bacterial examinations may be 
serviceable in confirming the diagnosis. There may be 
erythematous blotches or urticaria or petechial spots, which 
may be so grouped as to suggest a nervous origin. 

The urine usually contains small amounts of albumin and 
casts. There may be polyuria. Glycosuria has been observed 
in a certain number of cases. 

Digestive symptoms are not pronounced,.with the excep¬ 
tion of the initial vomiting. The bowels are usually obsti¬ 
nately constipated. In a few cases a complicating dysentery 
has been observed. The abdominal wall may be markedly 
retracted, presenting a “boat-shaped” appearance. There 
may be severe abdominal pain. 


EPIDEMIC CEREBROSPINAL MENINGITIS. 


99 


In the latter stages of the disease the symptoms of nervous 
excitation give way to those of nervous depression, and 
symptoms of cerebral compression make their appearance. 
The patient usually makes no more actual complaint of 
headache, although it is evident that there is still some 
pain experienced. There are increasing dulness and apathy, 
which may proceed to stupor and coma. There may be pe¬ 
riods of delirium, usually now of the low, muttering variety. 
Photophobia is succeeded by lack of perception of light; 
the pupils are usually dilated and do not react. Noises are 
not objectionable. The muscular twitchings and spasms 
give way to weakness and paralysis, which are most marked 
in the face and in the eye-muscles, producing strabismus. 
The temperature continues to be irregular. The respiration 
may be irregular, or even of the “ Cheyne-Stokes ” variety. 
The pulse is usually slower than would be expected from 
the prostration and the fever, becoming rapid and feeble, 
however, toward the close of the disease. The combination 
of fever, headache, slow pulse, and constipation is exceed¬ 
ingly characteristic of meningitis in any of its forms. At 
the close of the disease there may be diarrhoea and loss of 
the sphincter control. In fatal cases there may be ante¬ 
mortem hyperpyrexia. In cases that recover the fever 
gradually disappears, while other symptoms depart more 
slowly. 

The duration of ordinary cases is between one and three 
weeks, although more protracted cases are not uncommon. 

Anomalous cases are met with, especially in certain epi¬ 
demics. 

1. Course in Young Babies .—Convulsions are frequent at 
the outset and throughout the disease; the fever is high ; the 
pulse is rapid throughout; the child passes into stupor alter¬ 
nating with restlessness, and death in coma ensues. 

2. Mild Cases .—There are headache, nausea, vertigo, and 


100 


MANUAL OF THE PRACTICE OF MEDICINE. 


a little fever. There may be stiffness of the neck and vom¬ 
iting. The diagnosis of these cases is difficult except dur¬ 
ing epidemics. 

3. Intermittent Cases .—The regular course of the disease 
in these cases is marked by periods of improvement and 
remission of fever lasting for a few hours or days, the remis¬ 
sions recurring at regular intervals. The case may be mis¬ 
taken for malaria or pyaemia. 

4. Abortive Cases .—Here the disease begins in the regular 
way, but recovery is rapid after a few days. 

5. Malignant Cases .—The patient is suddenly attacked 
by a chill, headache, and high fever. The pulse is feeble and 
frequently is slow, and hemorrhagic spots usually appear on 
the skin. Cerebral symptoms develop rapidly, and death 
from toxaemia occurs in a few hours or days, before lesions 
or characteristic symptoms have time to develop. These 
cases are usually seen only in the most severe epidemics. 

Complications.—There may be bronchitis or broncho¬ 
pneumonia. Lobar pneumonia is frequently observed. 
There may be pericarditis, endocarditis, or pleurisy. There 
is usually conjunctivitis, but more serious lesions may de¬ 
velop, such as purulent keratitis or choroiditis with loss of 
sight, or optic neuritis with atrophy. Arthritis occurs in 
some epidemics, the joints being painful, red, and swollen 
from effusion in and around the joint-cavities, the effusion 
in some cases being purulent. 

Sequelae.—Convalescence, which is apt to be slow and 
tedious from prolonged muscular and mental weakness, 
may be complicated by relapses. In some cases the lesion 
in the lateral ventricles continues as a chronic hydrocephalus. 
The patient recovers partially from the acute attack, but a 
little fever remains, the pulse is feeble, and there is great 
gastric irritability. The pupils are usually dilated. Ema¬ 
ciation becomes extreme. The patient lies in apathy or 


EPIDEMIC CEREBRO-SPINAL MENINGITIS. 


IOI 


stupor varied by periods of restlessness and moaning. 
I hese cases last for weeks, and final recovery is rare. 

Some patients are left in a condition of bodily and mental 
weakness. They become anaemic, irritable, forgetful, and 
hysterical, usually recovering after a lapse of months. 

There may be paralysis from post-febrile neuritis. 

There may be sequelae Irom involvement of special senses. 
T here may be partial or complete blindness from corneal 
ulcerations, from choroiditis, or from atrophy of the optic 
nerve. Permanent deafness may result from perineuritis of 
the auditory nerve or from labyrinthine disease, many cases 
of deaf-mutism being due to this disease. 

The prognosis, which is bad, but not hopeless, depends 
not only on the severity of the symptoms, especially those 
of cerebral origin, but also on the general character of the 
epidemic, the mortality ranging from 20 to 75 per cent, in 
different epidemics. The average mortality is about 40 per 
cent. Endemic cases are usually less severe than those 
occurring during epidemics. 

Treatment.— The treatment is entirely symptomatic. In 
robust patients, if seen early at the outset, local bleeding by 
leeches applied to the temples or behind the ears, or the 
application of wet cups to the nape of the neck, is frequently 
of much benefit. Relief is usually afforded by the contin¬ 
uous application of cold, by the cold coil, or by ice-bags 
applied to the head or the spine. Large doses of ergot are 
frequently given in the earlier stages to diminish cerebral 
congestion, and iodide of potassium in 20-grain doses three 
times a day is warmly recommended throughout for its sup¬ 
posed “ absorbent ” action. 

Blistering is now considered injudicious, as it does no 
good and adds to the discomfort of the patient. Applica¬ 
tions to the shaven scalp of iodoform ointment and mercu¬ 
rial inunctions have not seemed to exert a favorable effect. 


102 MANUAL OF THE PRACTICE OF MEDICINE. 

For the nervous symptoms sedatives and even narcotics 
are required. Bromide of sodium, hyoscyamine, phenacetine, 
or small doses of atropine may be enough in mild cases, but 
the severer forms demand morphine, preferably by hypo¬ 
dermatic administration. 

High temperatures are to be combated by hydrotherapy, 
and every indication of heart weakness must be met by the 
free and judicious use of heart stimulants. 


DIPHTHERIA. 

Definition. —Diphtheria is an acute contagious disease 
due to infection by the Kdebs-Loeffler bacillus, and charac¬ 
terized by an exudative inflammation of mucous membranes 
or of abraded cutaneous surfaces, with constitutional symp¬ 
toms. 

Etiology. —The disease is endemic in all large cities, and 
frequently becomes epidemic, the most characteristic epi¬ 
demics occurring in summer hotels, in institutions, and in 
small villages. The spread of the disease is greatly favored 
by poor hygiene, bad plumbing, and the crowding together 
of people. It is contagious by personal contact, and may 
be transmitted by clothing, toys, bedding, etc., even after the 
lapse of months or of years, the germ having intense vital¬ 
ity and duration of life. Cases, however, in which the con¬ 
tagious property of the bacillus has been retained for more 
than one year, though reported in medical literature, are of 
questionable authenticity. 

It is doubtful whether the disease is communicable by the 
breath alone. It is known, however, that the greatest con¬ 
tagion is conveyed by the secretions and by loosened bits 
of membrane from the infected site coughed into the faces 
of the attendants or sucked from the tracheotomy wound 
by an over-zealous operator. The disease may be trans- 


DIPHTHERIA . 


103 


initted by kissing. Cases are reported in which the disease 
has been taken from diphtheritic animals, especially cats. 

The disease is usually one of childhood, one-half the cases 
occurring before the fifth year, although it is common enough 
in those under fifty. It may occur in young babies. One 
attack does not procure immunity. The exciting cause is 
now known to be a bacillus described in 1883 by Klebs and 
in 1884 by Loeffier, and bearing their combined names. Its 
length is a trifle less than the tubercle bacillus, but it is 
broader, with clubbed extremities. It is readily stained, 
shows a characteristic growth in nutritive media, and is 
capable of causing the disease in animals. Cultures are 
best made in blood-serum, colonies in agar-agar. It is 
destroyed by aqueous solutions of bichloride of mercury 
(1 : 8000), salicylic acid (1 : 2oco), and carbolic acid (1 : 50). 
It is destroyed also by boiling. The bacilli are usually 
found only in the pseudo-membrane, though exceptionally 
they may be present in the blood and in the viscera. They 
may persist in the throat for so long as three weeks after 
the attack, and are found in the throats of 25 per cent, of 
those who have been exposed to diphtheria. They are 
never found in other diseases. 

Infection usually occurs through slight abrasions of the 
mucous membranes, and is favored by diseased conditions 
of the upper air-passages. The diphtheritic ptomaine has 
been isolated, and its injection in animals has been followed 
by all the symptoms of diphtheria except the membrane. 

Immunity. —By the inoculation of attenuated cultures in 
some animals immunity has been secured ; and, what is more 
important, infected guinea-pigs have been cured by inocu¬ 
lating- them with the blood of the animals rendered thus 
immune. At the present time diphtheria in the human sub¬ 
ject is being treated by this method, with the result of 
reducing the mortality one-half. If these inoculations are 


104 MANUAL OF THE PRACTICE OF MEDICINE. 


begun by the second day of the disease, the patient almost 
invariably recovers. 

Pathology.—The essential lesion consists of a croupous 
inflammation of mucous membranes, more rarely of abraded 
cutaneous surfaces. The most frequent sites are the tonsils, 
pharynx, palate, nares, larynx, trachea, or bronchi, and less 
frequently the mouth, gums, lips, oesophagus, stomach, and 
vagina. 

The mucous membrane is congested, swollen, and infil¬ 
trated with fibrin-serum and pus, which appear on its free 
surface. The epithelial cells and the exuded leucocytes 
die and undergo hyaline degeneration, losing their nuclei— 
the so-called “ coagulation-necrosis ” of Weigert. There 
may be necrosis of the false membrane, and of the stroma of 
the underlying mucous membrane as well, which may be¬ 
come gangrenous in some cases. Erosion of large arteries 
with even fatal hemorrhage may result. 

If the patient recovers, the false membrane sloughs off en 
masse or by gradual disintegration, superficial ulcers being 
usually left. If the ulcers be deep, evident cicatrization 
may result. Successive crops of membrane form if the 
false membrane be forcibly detached. 

In the false membrane are found the characteristic bacilli 
associated with a variety of other organisms, especially 
streptococci and staphylococci, which, as a rule, penetrate 
more deeply than does the Klebs-Loeffler bacillus. 

The appearance of the membrane varies. It may be ad¬ 
herent, a bleeding surface being left after its forcible removal, 
or it may be shreddy and readily detached. It may be thick, 
soft, and yellow, or it may be thin and so transparent that 
it can hardly be seen by the naked eye, and in some cases 
there may be evident only a localized hyperaemia. It may 
be of a dirty-green color, or it may be putrid and gangren¬ 
ous. The surrounding mucous membrane is congested and 


DIPHTHERIA. 


105 


inflamed. These appearances are identical with those of 
pseudo-diphtheritic membranes, the only point of difference 
being the presence of the Klebs-Loeffler bacilli in the true 
cases. 

Complicating lesions are variable. There may be adenitis 
of the lymphatic glands near the infected area, which may 
proceed to suppuration from mixed streptococcus infection. 
The periglandular tissues, and even the salivary glands, may 
become in like manner affected. Bronchitis, either catarrhal 
or diphtheritic, areas of atelectasis, and patches of broncho¬ 
pneumonia are usually present in fatal cases. There may 
be endocarditis in rare cases, but an acute degeneration of 
the heart-muscle is not uncommon and may lead to sudden 
death. 

The kidneys may be the seat of an acute degeneration or 
of an exudative or a diffuse nephritis. The spleen may be 
found large and soft. In cases fatal from asphyxia the 
viscera are usually congested. 

Incubation may occupy from one to fourteen days, the 
average duration being from two to five days. 

The symptoms may be divided into two groups : 1. Gen¬ 
eral symptoms due to the ptomaine-poisoning, and which 
are the same in all cases; 2. Local symptoms , which vary 
according to the localization of the lesion. 

1. General Symptoms .—In some cases the disease begins 
abruptly with a chill or, in children, with convulsions. Usu¬ 
ally, however, the onset is insidious, being marked by pros¬ 
tration, fever, and often by digestive disturbances. 

The fever does not run a typical course; it may be as 
high as 104° F., but a temperature of from 101 c to 103° F. 
is more common. It is often irregular or intermittent, and 
possibly is altogether absent even in fatal cases. 

Prostration is an early and constant symptom, and is 
proportioned more to the actual gravity of the case than 


IO6 MANUAL OF THE PRACTICE OF MEDICINE. 

to the height of the fever or to the local lesion. In mild 
cases prostration may be slight or absent. The pulse is 
rapid, with a tendency to become feeble according to the 
severity of the disease. In some cases the pulse may be 
slow (50 to 60); this is not usually a favorable sign. At 
any time sudden or gradual heart failure may develop, even 
during advanced convalescence. This makes the prognosis 
uncertain in every case. 

Sudden heart failure will be followed by almost instanta¬ 
neous death. Gradual heart failure will be shown by increas¬ 
ing rapidity and weakness of the pulse, dyspnoea, cyanosis, 
and congestion of the different viscera, with death in a few 
hours or days. 

Cerebral symptoms comprise stupor, often alternating with 
restlessness, or mild delirium or convulsions, semi-coma, and 
coma. These symptoms are rather rare considering the 
severely toxic character of the disease. They may appear 
early, from the toxic action of the ptomaines on the nervous 
centres, or they may appear late, as the result of asphyxia. 

In some cases there appears an erythematous eruption 
resembling that of scarlatina. It is, however, evanescent, 
fading usually in a few hours. Bacterial examination of 
the pseudo-membrane or the exudate may be necessary to 
differentiate between this disease and those cases of scar¬ 
latina complicated with pseudo-diphtheritic pharyngitis. 
In malignant cases there may be purpura. Albuminuria 
occurs in the majority of severe cases, from parenchyma¬ 
tous degeneration of the kidney. The occurrence of a true 
nephritis must be considered as a complication. 

2. Local Symptoms. — (a) Tonsillar Diphtheria .—This is 
the commonest form of diphtheria, and at the same time the 
least serious. There are three clinical forms: 

(1) There is a pseudo-membrane on one or both tonsils, 
having no relation to the crypts. (2) The crypts of the 


DIPHTHERIA. 


IO; 

tonsils are filled with a pseudo-membranous exudate which 
appears on the surface as white points, resembling in every 
way the appearances presented by ordinary follicular tonsil¬ 
litis, and from which it can be differentiated only by bacterial 
examination. These white points in some cases may so 
coalesce that the tonsils are covered with irregular white 
patches. (3) The tonsil swells; there are swelling and 
oedema of the surrounding structures, resembling the ap¬ 
pearances of ordinary suppurative peritonsillitis or quinsy. 
No membrane is visible until after thirty-six to forty-eight 
hours. These cases, which seem to be due to bacterial 
invasion of the deeper structures, are" apt to do badly. 

The local symptoms of the first two varieties are apt to be 
mild, lasting but a few days. There may be moderate fever ; 
prostration is slight or absent; the voice is muffled ; there are 
pain and soreness, which are increased by talking or swal¬ 
lowing. 

However mild the case, the disease may spread and 
become severe, or it may be followed by any of the com¬ 
plications or sequelae, and it may be the cause of infecting 
others even with the most severe forms. 

(b) Pharyngeal Diphtheria. —(1) There may only be an area 
of local hyperaemia without any pseudo-membrane. This 
condition is seen in those exposed to diphtheria, and is 
commonly called “ sympathetic sore throat.” It is really 
diphtheritic, however, and may not only be followed by 
sequelae or the spread of the disease, but may even be the 
source of contagion to others. 

(2) There may be a pseudo-membrane evident, usually 
associated with membrane on the tonsils. 

Symptoms .—In mild cases there may only be malaise, 
slight fever, and a raw feeling in the throat. In severer 
cases there may be pain, increased by talking or by swallow¬ 
ing, muffled voice, fetid breath, and in some cases ptyalism. 


108 MANUAL OF THE PRACTICE OF MEDICINE. 

(3) Nasal diphtheria is not common. It is rare as a 
primary form, being usually secondary to membrane in the 
pharynx. From the formation of pseudo-membrane in the 
nasal cavities and the attendant swelling of their mucous 
membranes the nostrils become more or less occluded. 
There is usually a discharge from the nose of muco-pus or 
sero-pus, which may be stained with blood. In some cases 
there is a brown, watery discharge which stains the pillow 
and excoriates the lips. 

The glands of the neck are more often involved in naso¬ 
pharyngeal diphtheria than in any other form, considerable 
deformity usually resulting from their tumefaction. 

If the nose be involved, the patient is apt to do badly. 
Death usually results from sepsis with cerebral symptoms 
or from heart failure. Small babies either asphyxiate or 
starve from their inability to breathe if they are nursed, 
unless they are fed by the stomach-tube. 

(4) Laryngeal diphtheria is a common form, and is greatly 
dreaded for the following reasons: 

(a) There is apt to be asphyxia from the occlusion of the 
glottis by pseudo-membranes, by the swelling and oedema 
of the vocal cords, and in some cases by their paralysis, 
from the projection of little tongues or tags of loose pseudo¬ 
membrane into the rima glottidis, and by the spasm from 
time to time of the laryngeal muscles. 

(h) As the larynx is seldom infected primarily, but is 
affected from the spread of the disease from the pharynx, 
the pseudo-membrane is apt to be extensive and toxaemia 
severe. 

(e) The pseudo-membrane is apt to spread downward and 
to involve the trachea and the bronchi. 

(d) There is apt to be developed either septic broncho¬ 
pneumonia or “deglutition-pneumonia” or areas of atelec¬ 
tasis. 


DIPHTHERIA . 


IO9 


(e) Because the larynx is affected usually in children, who 
do not stand the disease well. 

Symptoms .—The voice is hoarse and croupy, and may be 
reduced to a faint whisper. There is a hoarse, croupy 
cough. The breathing is rapid and inefficient, and there is 
obstructive dyspnoea which may be either obvious or 
masked. 

In obvious dyspnoea the child sits up with the neck craned 
forward, to bring into play all the accessory muscles of 
respiration. The alae nasi dilate; inspiration is prolonged and 
stridulous. There is inspiratory sinking of the spaces above 
and below the clavicles. The face is anxious and distressed, 
and may be semi-cyanotic. From time to time there occur 
paroxysms of increased dyspnoea that are often relieved by 
coughing up pieces of pseudo-membrane. Unless the con¬ 
dition is relieved by the casting off of the pseudo-mem¬ 
brane or by operative interference, the child passes into the 
condition of masked dyspnoea. 

In masked dyspnoea the child no longer struggles for 
breath, but lies flaccid or in a stupor which may deepen into 
coma. The skin becomes cold and livid, the pulse becomes 
more rapid and feeble. In this condition the patient may 
remain for from one to four days, and recovery from this 
stage is exceedingly rare. All cases, however, do not pass 
into this stage, but after a time the pseudo-membrane be¬ 
comes loosened and is coughed up either in large pieces or 
by gradual disintegration. Glandular swellings are not 
seen in diphtheria of the larynx alone. 

Complications and Sequelae.—Local complications have 
already been alluded to. They are sloughing, erosion of 
arteries with hemorrhage, and swelling of the neighboring 
glands. 

Pulmonary complications occur in almost all fatal cases, 
and present their ordinary symptoms and physical signs. 


IIO MANUAL OF THE PRACTICE OF MEDICINE. 

Should pneumonia occur in very sick patients, its symptoms 
are frequently masked by those of the primary disease. 

There may be gastritis or enteritis. Renal complications 
are common. 

Acute parenchymatous degeneration shows itself by 
changes in the urine alone. Acute exudative or acute dif- 
fuse nephritis may occur during the disease or during con¬ 
valescence. There are the changes in the urine common to 
such lesions; there maybe suppression with uraemic symp¬ 
toms. In some patients much exhausted by the disease 
uraemic symptoms may not appear. 

Of the sequelae, peripheral neuritis is the most important. 
It is seen in from io to 40 per cent, of all cases, according 
to the epidemic, and usually occurs in the second or third 
week of convalescence. It may follow either mild or severe 
cases. 

The muscles most frequently paralyzed are those of the 
soft palate. The voice becomes nasal, there is inability to 
clear the throat, and deglutition is interfered with, fluids 
regurgitating through the nose. This may be the only 
symptom. The patient may have to be fed through the 
stomach-tube, especially if the paralysis extend to the con¬ 
strictors of the pharynx. 

The next most common forms are paralyses of the eye- 
muscles. The intrinsic muscles may be affected, causing 
dilatation of the pupil and loss of power of accommodation. 
The involvement of the extrinsic muscles produces ptosis 
and strabismus. 

If the muscles of the larynx be affected, there will result 
dyspnoea, aphonia, and a croupy cough. 

More rarely the muscles of one or more extremities may 
become paralyzed, or there may only be some weakness 
in the legs with loss of tendon-reflex. 

Diphtheritic paralysis usually lasts but a few weeks or 


DIPHTHERIA. 


I I I 


months, terminating in recovery, although in some cases 
it may become permanent. 

The nephritis may become chronic and lead to the death 
of the patient. There may be resulting endocarditis. If 
the conjunctivae be the seat of a pseudo-membrane, ulcers 
of the cornea with opacities usually result. 

The prognosis is always serious, and must in all cases 
be made guardedly, because, however mild the attack may 
be, it may at any time spread and become severe. The dan¬ 
ger of heart failure must always be regarded. The progno¬ 
sis depends upon the character of the prevailing epidemic 
and also upon the age of the child, 42 per cent, of cases 
being fatal before the fourth year, 35 per cent, between the 
fourth and tenth years, and 10 per cent, between the tenth 
and twentieth years. The average mortality is about 25 per 
cent. The prognosis depends not only upon the severity 
of the general infection, but also upon the locality and extent 
of the lesions, being worse in nasal, laryngeal, pharyngeal, 
and tonsillar cases in the order mentioned. The prognosis 
also depends upon the presence of complications and upon 
possible sequelae. As a rule, a good prognosis may be 
given to cases of tonsillar diphtheria that do not spread 
within two days. 

The mortality has been reduced within the past year, 
under the antitoxine treatment, to just one-half the former 
death-rate. If cases can be treated by antitoxine within 
the first thirty-six hours, the mortality will still further be 
reduced. 

Treatment. —Prophylactic Treatment .—Careful isolation 
should be enforced, not only for the patient, but also, as 
far as possible, for the attendants. “ The members of a 
household in which a case of diphtheria exists should be 
regarded as sources of danger unless cultures from their 
throats show the absence of virulent diphtheria bacteria.” 


I 12 MANUAL OF THE PRACTICE OF MEDICINE. 

(Park). Attendants on the sick should have their throats 
irrigated every four hours with a 1:10,000 bichloride solution. 
Isolation should be continued until the bacilli are proved to 
be absent. In one-half the cases the bacilli disappear within 
three days after the disappearance of the pseudo-membrane ; 
in one-third of the cases, in seven days ; in one-tenth of the 
cases, in fourteen days ; while the bacilli may remain in a 
small percentage of cases as late as the sixty-third day. 
After isolation is relaxed, the room, with the bedding, toys, 
etc., should be fumigated thoroughly with sulphur, and the 
linen should be boiled in 2 per cent, carbolic solution. The 
walls and the floors should be scrubbed with 1 : 10,000 
bichloride solution. 

General Treatment .—The child should be put to bed and 
be kept on a milk diet. The temperature of the room 
should be 75 0 F., and the air should be kept moist. The 
use of the steam-tent will be alluded to. Careful attention 
should be paid to the heart, and stimulants should be given 
freely when required. Especially are alcoholic stimulants 
to be recommended. The danger of heart failure during 
early convalescence should not be forgotten. The temperature 
may be controlled, if necessary, by hydrotherapy. Internal 
antipyretics should be avoided. Large repeated doses of 
the tincture of the chloride of iron (4 to 5 drops hourly 
to a child of three years) and the use of corrosive sublimate 
in small doses (gr. ^ every four hours as a limit, or gr. -g 1 ^- 
every hour) have been recommended warmly. The former 
is recommended, with alcoholic stimulants, as a routine treat¬ 
ment. Chlorate of potash should not be employed, because 
of its evil effect upon the kidneys. 

Local Treatment .—As diphtheria is a local disease at first, 
the bacilli growing in the pseudo-membrane and elaborating 
there the toxalbumins that poison the system, local treat¬ 
ment becomes of the first importance in destroying the activ- 


DIPHTHERIA 


Plate 9 



Irrigation of naso-pharynx (Berg) 



















DIPHTHERIA. 


113 


ity of the germ and in removing the toxalbumins when 
formed. Rough treatment and the mechanical tearing off 
of the pseudo-membrane are of actual harm. The best 
treatment consists in the thorough irrigation of the throat 
and nose with a neutial salt-solution (,3j to Ojj or with 
boric-acid solution, a tablespoonful to the pint. A foun¬ 
tain syringe should be used, and the fluid should be at a 
temperature of 85° F. The patient lying on the side (as 
in Plate 9), the nozzle of the irrigator should be inserted 
in the upper nostril until the fluid runs out of the other 
nostril and the mouth. Then the process is repeated with 
the lower nostril. The tip of the irrigator should then be 
passed well back over the dorsum of the tongue, and the 
pharynx well flushed out. In case the nostrils be occlud¬ 
ed with membrane, the fountain syringe may be elevated 
six or eight feet. Such irrigation should be done every 
two hours. In septic cases irrigation with bichloride 
(1 14000 to 1 : 8000) may be employed every four to eight 
hours in addition. If the membrane be thick, insufflations 
of papoid powder may be used to advantage. Other local 
remedies have been recommended, but are not now as much 
used as formerly. Among these remedies are insufflations 
ot powdered sulphur, applications of tincture of the chlo¬ 
ride of iron, iodine, peroxide of hydrogen, trypsin, and 
lactic acid. 

So high an authority as Loeffler recommends the follow¬ 
ing method of local treatment: After cleansing the surface 
of the pseudo-membrane the following solution is to be ap¬ 
plied on cotton swabs for ten seconds every three hours, 
later three times a day: 

3 ^. Alcohol, 60 volumes; 


Toluol, 

Liq. ferri sesquichlorati, 


36 volumes; 

4 volumes ; 
20 volumes. 


Menthol 


8 


114 MANUAL OF THE PRACTICE OF MEDICINE. 


In laryngeal diphtheria with dyspnoea two additional rem¬ 
edies are warmly recommended—the steam-tent and calo¬ 
mel fumigation. 

The steam-tent should be used upon the first appearance 
of dyspnoea, but it may be used in any case as a routine 
measure. A good way to form the tent is to throw sheets 
over clothes-horses arranged about the bed, or to suspend 
from the ceiling an open umbrella about which the sheets 
can be draped. The nozzle of a steam-kettle should be in¬ 
serted within the tent, so that the air is kept constantly 
moist. 

Calomel inhalations are employed in laryngeal diphtheria, 
especially with dyspnoea: io to 20 grains may be used 
every two to four hours without danger of salivation to a 
child, although the nurses may suffer from sore gums; mer¬ 
curic diarrhoea may, however, occur. The calomel should 
be piled on a piece of tin resting upon the sides of a small 


pail or chamber utensil, un¬ 
der the centre of the tin be¬ 
ing the alcohol lamp (Fig. i) 
The whole apparatus is to be 
placed inside the croup-tent, 
and care must be exercised 
that the child does not kick 
the lamp over and set fire 
to the bedding. 



When the laryngeal pseudo¬ 
membrane is being loosened, 


Fig. i.—Method of fumigating with caio- its separation may be hast¬ 


mel: a, pail (section); b, alcohol; c, strip 
of bent tin ; d, pile of calomel powder. 


ened by emetics; but these 
are not to be recommended 


except in robust cases with good heart-action, in whom 
dyspnoea appears due to the obstruction caused by the loose 
membrane and the mucous secretion. 







DIPHTHERIA. 


Plate io. 



2 



Klebs-Loeffler bacillus (photographed by Dr. W. H. Park). 2. Hutchinson teeth. 
































DIPHTHERIA. 


US 

When actual obstructive dyspnoea begins the question of 
operative interference comes into consideration. For the 
details of intubation and tracheotomy the reader is referred 
to works on surgery. It seems that intubation should be 
our first choice, and it should be done as soon as slight 
cyanosis appears. 

Scrum-therapy .—The growth of the Klebs-Loeffler bacillus 
(Plate io) in the body-tissues develops the peculiar toxalbu- 
min to the poisoning from which the constitutional symptoms 
are due. Nature in some unknown way elaborates in the body 
an antidotal poison, the antitoxine, and when the two poisons 
balance in effect the constitutional symptoms cease and the 
patient recovers. If antitoxine can be made outside the 
body, and injected when needed, in sufficient doses, without 
waiting for the system to elaborate it, the disease, it was 
thought, might be stamped out at the onset. The growing 
experiences of the past year tend more and more to prove 
the correctness of this assumption. 

The method by which the antitoxine is obtained is as 
follows : All animals susceptible to diphtheria can be ren¬ 
dered immune by injecting into their bodies pure cultures 
of the bacillus in gradually increasing virulence. Weaken¬ 
ing of the toxine is effected by diluting it with iodine solu¬ 
tions. For various reasons the horse is the most satisfac¬ 
tory animal for the purpose. 

When immunized, the blood-serum contains a large quan¬ 
tity of antitoxine and can be used for subcutaneous injec¬ 
tions in human diphtheria. A small quantity of tricresol is 
added to the serum to keep it from decomposing. Three 
reliable serums are in the market—Roux’s, Behring’s, and 
Aronson’s. Each serum supplies a weaker (“ immunization 
serum ”) and a stronger solution. 

The dose of antitoxic serum varies with the size and the 
weight of the patient, the virulence of the disease, and the 


I 16 MANUAL OF THE PRACTICE OF MEDICINE . 

length of time since the onset of the symptoms. The ordi¬ 
nary dose of the weaker or immunization serum is 20 cubic 
centimeters as a single injection, given in the skin between 
the shoulders or in the flank. A subsequent injection of 10 
cubic centimeters may be given in twenty-four hours if the 
Klebs-Loeffler bacilli are found present. Ordinarily two 



such injections suffice for recovery. A red rash may follow 
such injections. Under this treatment the temperature rap¬ 
idly falls, the membrane rapidly disappears, and early con¬ 
valescence is established (see Fig. 2). 

It is believed that recovery should take place in all 
patients treated within the first twenty-four hours. Taking 

















































































































ER YSIPELAS. 


II 7 

all the cases together, the mortality has been reduced one- 
half, and with improved methods and improved apprecia¬ 
tion oi the value of early diagnosis and early treatment the 
mortality will still further be reduced. 

ERYSIPELAS. 

Definition.—Erysipelas is an infectious inflammation of 
the skin with constitutional symptoms, caused by the inocu¬ 
lation of the streptococcus erysipelatosus. 

Etiology.—The disease is due to infection of the lym¬ 
phatics of the skin by a streptococcus which is identical 
in appearance with the streptococcus pyogenes. Infection 
always occurs through wounds or abraded surfaces, intact 
skin and mucous membranes affording absolute protection. 
Two forms are usually described— (a) a traumatic form 
complicating surgical wounds and injuries, and (/;) an idio¬ 
pathic form occurring usually in the face, in which no trau¬ 
matic point of origin can be found. The only real differ¬ 
ence between these two forms is that in the one the point 
of entrance is apparent, while in the other it is slight and is 
usually overlooked. The disease is favored by poor hygiene, 
by bad plumbing, and by contact with infected cases. As 
inoculation through abraded surfaces is necessary to cause 
the disease, it cannot be considered as contagious in the 
ordinary acceptation of the term. It is commonest in alco¬ 
holic and debilitated patients and in those suffering from 
Bright’s disease. One attack does not secure immunity. 
Some patients are exceedingly susceptible and may suffer 
from repeated attacks. 

Pathology.—Erysipelas is really a progressive lymph¬ 
angitis of the skin involving the perilymphatic tissues by 
continuity. There is an infiltration of the cutis vera by 
fibrin serum and leucocytes ; this infiltration in severe cases 
may extend to the subcutaneous connective tissue. The 


1 18 MANUAL OF THE PRACTICE OF MEDICINE. 


lymphatics are crowded with the streptococci, especially at 
the margin of the patch and extending into the healthy 
skin. Vesicles and bullae may be formed. Suppuration 
does not occur unless there be an added infection by pus 
microbes. 

Symptoms begin from fifteen to sixteen hours after inoc¬ 
ulation. 

General Symptoms .—The disease usually is initiated by a 
chill and a rise of temperature to 103° or 104° F. or even 
higher. Nausea and vomiting are common at the onset. 
The pulse is full and bounding, and is rarely over 100 except 
in the most severe forms or in debilitated and alcoholic sub¬ 
jects. In these cases the pulse may become rapid and feeble 
and may be a source of real danger. 

Delirium belongs to the severer cases, and is especially 
marked in alcoholic patients. It may be either mild and 
maniacal or low and muttering. There is usually severe 
headache, especially in erysipelas of the face and scalp. 
Prostration is marked in proportion to the severity of the 
disease. There may be albuminuria. In fatal cases the 
patient may pass into a “typhoid condition.” 

The constitutional symptoms may be mild, such as would 
be due to a slight local inflammation, or they may be ex¬ 
ceedingly well developed, resembling those caused by any 
severe general infection. 

Local Symptoms .—The skin becomes swollen and shiny 
and of a rose color which disappears on pressure. It is dis¬ 
tinctly thickened and indurated. The patient complains of 
feelings of tension, burning, and itching. The swelling is 
most marked in places where there is considerable loose 
connective tissue, as in the face or the eyelids, and in these 
localities there is also considerable oedema. Inflammatory 
changes are more marked at the border of the eruption, 
which is abrupt and elevated and shows tongue-like pro- 


ER YSIPELAS. 


1 19 

longations projecting into the healthy skin. These cha¬ 
racteristics of the border of the patch are distinctive and 
absolutely diagnostic. In some cases there appear vesicles 
or bullae. 

If there be an added infection by the ordinary pus 
microbes, the contents of the vesicles or the bullae may be¬ 
come purulent, or there may be complicating phlegmonous 
inflammation of the deeper structures of the skin, or meta¬ 
static abscesses of internal viscera, or septic inflammation 
of any of the serous membranes. In some cases the local 
inflammation is so intense that superficial gangrene results. 
Exfoliation of the skin usually follows the subsidence of the 
eruption. 

When the disease once begins, it is common for it to 
spread from the periphery, so that large surface areas may 
become successively involved. Its progress may be checked 
by any decided fold in the skin, particularly the naso-labial 
fold. It is frequently limited at the border of the hairy 
scalp. In facial erysipelas the chin and the anterior aspect 
of the neck are never affected. In some cases erysipelas 
shows a tendency to creep from place to place, subsiding 
in the old situations while new areas are constantly becom¬ 
ing invaded. In this way it may spread over most of the 
body and the extremities. This form is often described as 
“erysipelas migrans.” In other cases the erysipelatous 
inflammation may attack a part far separated from the pri¬ 
mary seat of infection. This condition may result either 
from infective embolism or by auto-inoculation, the cocci 
being carried from the primary site and being inoculated 
through a scratch or an abrasion into the distant part. These 
cases are designated “ metastatic erysipelas.” 

If the streptococci obtain entrance to the lymphatics of 
the post-partum uterus, the most virulent and fatal form 
of puerperal sepsis results. 


120 MANUAL OF THE PRACTICE OF MEDICINE. 


The ptomaines of the erysipelas streptococci often exert 
a favorable effect on neoplasms, causing destruction of 
tumor-cells. Cases of cure of sarcoma, carcinoma, lupus, 
lipoma, and keloid have been reported. This effect may be 
produced either by an attack of erysipelas, accidentally or 
purposely induced, or by subcutaneous injections of the 
filtered or sterilized cultures of the streptococci into or near 
the tumor. Attacks of erysipelas in patients suffering from 
diphtheria have often exerted a beneficial effect on that 
disease. 

Complications are most commonly due to an added in¬ 
fection by pus microbes. There may be suppurative cellu¬ 
litis or suppurative thrombo-pyelitis. Metastatic abscesses 
in the viscera may occur, especially in the brain and lungs. 
There may be septic inflammation of serous membranes, 
meningitis being the most important, due usually to 
infection through the sheaths of blood-vessels or nerves 
from the face. There may be ulcerative endocarditis or 
pericarditis. Pleurisy is not uncommon with erysipelas 
of the chest-wall. Pneumonia and nephritis are infrequent. 

The prognosis is usually good except in debilitated sub¬ 
jects. The disease is usually fatal only by its complications. 

Treatment.— Prophylactic .—The patient should not be 
attended by those who have to do with puerperal or surgical 
cases. The attendants must carefully protect any abrasions 
on their own persons, and must cleanse the hands frequently 
with an antiseptic solution. In hospitals the patient must 
be isolated and the ward and bedding be disinfected care¬ 
fully. In private practice rigid isolation is not so neces¬ 
sary. 

General treatment consists in careful nursing and feeding 
and in controlling annoying or threatening symptoms on 
general principles. Stimulants may be given freely in cases 
with enfeebled heart-action, and in these cases the admin- 


PYALMIA. 


121 


istration of camphor in doses of gr. i-ij every hour, as 
recommended by Pirogoff, has been found serviceable. As 
a routine treatment tincture of the chloride of iron is fre¬ 
quently given in large doses (oss in glycerin and water every 
two to three hours), but it does not seem to exert any spe¬ 
cific effect, and its efficacy is doubtful. 

Local treatment is to be resorted to in all cases, not only 
to relieve the local symptoms, but also to check further 
advance of the disease. Hueter recommends the injection 
of a 2 per cent, solution of carbolic acid under the healthy 
skin near the advancing border. Injections of weak solu¬ 
tions of bichloride or biniodide of mercury may be 
employed in like manner. Kraske recommends multi¬ 
ple scarification of the skin in advance of the lesion, with 
subsequent moist sublimate dressings. Painting the ad¬ 
vancing margin twice a day with a io per cent, solution of 
carbolic acid in alcohol is a simple measure, and the result 
is often brilliant. The spread of the disease may at times 
be checked by compression of the healthy skin at the pe¬ 
riphery by adhesive straps. 

To relieve the burning and itching, applications of cold 
water, of solutions of acetate of alumina, or of weak car- 
bolized or sublimate solutions may be employed, but hot 
applications are generally more grateful and seem to exert 
a beneficial effect upon the disease itself. Hot lead-and- 
opium solution or any of the above-mentioned solutions 
may be employed. Ichthyol in ointment or in collodion, 
though recommended, is not of much service. 

Abscesses and suppurations are to be treated without 
delay on general surgical principles. 

PYAEMIA. 

Definition.—Pyaemia is a septic disease characterized by 
repeated chills, a remittent or intermittent temperature, and 


122 MANUAL OF THE PRACTICE OF MEDICINE. 


metastatic abscesses in various parts of the body, due to 
emboli infected by the microbes of pus. 

Etiology.—Pyaemia can result only from suppuration in 
some part of the body, the microbes of suppuration (strep¬ 
tococcus pyogenes and the forms of staphylococci) being 
necessary for its development. There must always be, in 
the neighborhood of the focus of suppuration, an inflamma¬ 
tion of a vein due to the invasion of its wall by the micro¬ 
organisms. This phlebitis is regularly followed by the for¬ 
mation of a clot in the interior of the vein; into this clot the 
pus microbes make their way, as the result of which the clot 
becomes softened and breaks down, so that small pieces 
containing the microbes are swept into the general, circula¬ 
tion until they enter some vessel too small to allow their 
passage. Here they will become lodged, and as the nutri¬ 
tion of the part suffers from the cutting off of its blood-sup¬ 
ply by the emboli, the most favorable conditions are afforded 
for the development of metastatic foci of suppuration. 

The infecting emboli, to get into the arterial circulation, 
must first pass through the lungs, which act as filters. 
Hence the lungs are most frequently affected. If the emboli 
enter the arterial circulation, they may cause abscesses in 
any part of the body. This is the case also in malignant 
endocarditis, in which disease vegetations from the diseased 
valves containing micro-organisms become detached, are 
swept into the arteries, and produce metastatic abscesses in 
whatever part of the body they happen to lodge. The term 
“arterial pyaemia” is often used to designate these cases. 

Should the primary focus of suppuration occur in the 
district of the portal vein, multiple abscesses of the liver 
are produced, and there may be also suppurative pyle¬ 
phlebitis. 

In some cases the primary suppurative focus is so slight 
as to be overlooked. The term “ idiopathic pyaemia ” is 


P VALMIA. 


123 


used to designate these cases. Osteomyelitis, gonorrhoea, 
and prostatic abscess are the conditions most frequently 
overlooked. 

Symptoms.—The symptoms of septicaemia, and possibly 
the local symptoms of thrombosis of a vein near the sup¬ 
purating wound, may precede the actual symptoms of the 
disease. 

The onset is marked by a chill, which is repeated at regu¬ 
lar or irregular intervals throughout the disease. The tem¬ 
perature rises rapidly during and after the chill to 103° to 
105° F., and runs an intermittent or remittent course, its fall 
being accompanied by profuse sweating. There may be 
vomiting and diarrhoea. The pulse becomes rapid and 
feeble, and there is rapid emaciation. Delirium is infrequent, 
the mind usually being clear throughout the disease. The 
breath has a peculiar sweetish odor. There may be a septic 
erythema which is transitory. The face may be pale or 
there may be developed a moderate jaundice, usually of 
haematogenous origin. The spleen is usually large, and it 
may be painful and tender. There may be albumin and 
blood in the urine. 

The symptoms of the metastatic abscesses depend upon 
their number, size, and locality. Abscesses in the lungs 
usually give rise to cough and dyspnoea. 

Any of the serous membranes of the body may become 
secondarily affected, and septic involvement of the joints 
(pyaemic rheumatism) is common. 

The prognosis is always grave. Almost all patients die 
in a few weeks. In rarer cases the disease may be protracted 
for months. 

Diagnosis.—The three conditions with which this dis¬ 
ease is apt to be confounded are malaria, typhoid fever, 
and acute miliary tuberculosis. 

In malaria the chills, fever, and sweating occur with more 


124 MANUAL OF THE PE AC TICE OF MEDICINE. 


regular periodicity, are checked by quinine, and in the 
blood the plasmodium malariae can be found. 

A careful review of the case, the occurrence of spots and 
abdominal symptoms, and the course of the disease distin¬ 
guish it from typhoid fever. 

In acute miliary tuberculosis the symptoms are more 
those of septicaemia : there are usually evidences of tuber¬ 
cular foci, and bacilli are usually present in the sputum. 

Treatment consists in the aseptic treatment of all wounds, 
the early evacuation of abscesses if possible, and supporting 
the strength of the patient by feeding, nursing, and the 
administration of alcoholic stimulants in full doses. Qui¬ 
nine in large doses may be found of temporary benefit in 
controlling the fever, but it is of no actual service in modi¬ 
fying the disease itself. 

SEPTICAEMIA. 

Definition and Synonym. —Septicaemia is the train of 
symptoms resulting from the introduction into the circula¬ 
tion of septic micro-organisms or their ptomaines. Syn¬ 
onym : Sepsis. 

Septicaemia occurs in two distinct forms : 

1. “Septic intoxication is caused by the absorption of a 
pre-formed ferment or toxine which produces the maximum 
effect as soon as it reaches the circulation, and the symp¬ 
toms subside with the arrest of further supply and the 
elimination of the septic material from the circulation. 

2. “ Septic infection , on the contrary, occurs in conse¬ 
quence of the introduction into the circulation of living 
micro-organisms which multiply with great rapidity in the 
blood—a circumstance which imparts to this form of septi¬ 
caemia its progressive character ” (Senn). 

Clinical Forms.— i. Fermentation Fever (Resorption 
fever, Aseptic fever, or After-fever) is that form of septic in- 


SEPTICEMIA. 


125 


toxication which results from the absorption of the products 
of aseptic tissue-necrosis. It follows aseptic wounds or in¬ 
juries, especially if strong antiseptic solutions have been em¬ 
ployed, causing necrosis of the superficial tissues. It may fol¬ 
low transfusion of blood or of simple saline solutions, and it 
has been produced in animals by the intravenous injection 
of digestive ferments. It frequently follows extravasations 
of blood, especially if they be confined under high tension. 

Symptoms .—Within several hours after an operation or 
injury the temperature rises rapidly, frequently to 103° or 
IO4 0 F., subsiding in from one to three days. Constitutional 
symptoms are slight or absent. The early occurrence of 
fever differentiates this from the remaining forms of sepsis. 

2 . Sapr/emia is that form of septic intoxication resulting 
from the absorption of the products of putrefaction. For 
its development three conditions are necessary: (1) Dead 
iissiie, as clots in wounds or injuries, retained clots or prod¬ 
ucts of conception in the uterus after abortion or labor, or 
tissues devitalized by traumatism, irritants, or the action 
of bacteria. (2) Infection by putrefactive organisms com¬ 
prising various forms of bacteria or of the proteus groups; 
(3) Sufficient time must elapse for the generation and absorp¬ 
tion of ptomaines—at least twenty-four hours. 

Symptoms .—The first symptom is usually a chill, which is 
followed by a rise in temperature to 102° or 104° F. The 
pulse becomes rapid and weak, depending on the gravity 
of the case. Cerebral symptoms are common—headache, 
restlessness, and delirium. Vomiting and diarrhoea are 
almost constant in grave cases. The tongue is dry and 
often glazed, and may assume the “ dried-beef” appear¬ 
ance. The intensity of the symptoms depends on the 
amount of absorbed ptomaines. 

The diagnosis is rendered easy by the detection of the 
putrefactive focus by the sense of smell, fetor being constant. 


126 A/AJVUAL OF THE PRACTICE OF MEDICINE. 


The prognosis depends upon the amount of poison ab¬ 
sorbed and upon the possibility of removing the putrefying 
dead tissue by surgical treatment. 

3 . Progressive Septicaemia is that form of sepsis caused 
not only by the absorption of ptomaines produced at the 
site of the primary infection, but also of ptomaines produced 
in the blood from the microbes which it contains. The 
ordinary pus microbes are the most frequent causes of this 
form of septicaemia. 

Symptoms usually arise within twenty-four hours, seldom 
as late as the third day. An initial chill is common. The 
temperature is variable : usually the fever begins gradually, 
reaching finally 103° or 104° F., and often it is intermittent 
or remittent. In some cases the temperature may be subnor¬ 
mal. Prostration is an early symptom. The pulse becomes 
rapid, weak, and compressible. There is usually mental 
apathy and indifference, the expression being stolid. There 
may be drowsiness, stupor, or delirium. The face is pale or 
of a yellowish tinge. Vomiting and diarrhoea are marked 
in severe cases. The tongue is dry, red at the edges, black 
on the dorsum. In severe cases there may be capillary 
hemorrhages. 

The outlook is serious, depending upon the severity of the 
infection and the possibility of an early disinfection of the 
primary 'point of infection, preventing further ingress of 
microbes into the circulation. 

Fatal cases rarely last longer than one week, and in most 
severe forms death may ensue within twenty-four hours. 

CHOLERA. 

Definition and Synonym.—Cholera is an acute infectious 
disease caused by the comma bacillus and characterized 
by purging and collapse. Synonym: Asiatic cholera. 

Etiology.—The disease is endemic in India, a large num- 


CHOLERA. 


127 


ber of cases occurring every year, especially at the places 
of pilgrimage along the banks of the Ganges and Brahma¬ 
putra Rivers. From time to time it makes epidemic excur¬ 
sions to all civilized countries, where, after remaining a 
certain period, the epidemic ceases and the disease is found 
again only in India. Thus in 1884-86 it spread from India 
to Egypt, Italy, Spain, the south of France, Paris, Hungary, 
and the Argentine Republic ; it then disappeared, reappear¬ 
ing in 1892 in Persia, whence it had been carried from India 
by Mohammedan pilgrims, spreading rapidly to Russia, 
Germany, Franee, and Italy. A few cases brought on Ger¬ 
man and Italian steamers were seen in New York, but pro¬ 
tection was afforded by strict disinfection and quarantine. 

Epidemics spread along lines of travel, the infection being 
conveyed not only by those suffering from the disease, but 
also by freight, rags, bedding, etc. which have become con¬ 
taminated by infected fecal discharges. The infection is not 
carried by the air. The epidemics travel slowly, and they 
can be prevented by efficient quarantine and disinfection. 
They are favored by poor hygiene, especially by imperfection 
of the water-supply, by dirty habits, and by the crowding 
together of people. Any condition leading to diarrhoea pre¬ 
disposes to infection, and for this reason the epidemics regu¬ 
larly are more severe in warm seasons. Cold weather may 
modify an epidemic or check it temporarily, but does not 
entirely eradicate it. 

The exciting cause is a bacillus, the “comma bacillus” 
or the “ bacillus of Koch.” This bacillus is one-half the 
length of the tubercle bacillus, and of a curved or letter S 
shape. It is really a spirillum. It can readily be cultivated 
and can reproduce the disease. It is killed by boiling, by 
drying, and by acids, but it is not destroyed by freezing. 
It occurs in the intestinal discharges (though not when the 
stools become normal, nor in the diarrhoea of convalescence), 


128 MANUAL OF THE PRACTICE OF MEDICINE. 


occasionally in the vomita, in the intestines (whence it pene¬ 
trates into the intestinal lymphatics), and in the submucosa. 

The disease is not personally contagious, as it can occur 
only when the germ finds access to the intestinal tract, this 
entrance is accomplished through contaminated water or 
food. Nurses or washerwomen who deal with soiled bed- 
linen and who are uncleanly as to their hands may contam¬ 
inate their food in this way. 

Pathology.—There are no characteristic lesions except 
the presence of the bacilli. Bacteriological examinations 
should therefore be made in all doubtful cases. The body 
remains warm for a considerable time, and there is a marked 
post-mortem rise in temperature. Rigor mortis develops 
early and is well marked. There may be post-mortem 
movements of the body, arms, or legs. All the tissues are 
dry and anaemic; the blood is dark and thick; the serous 
membranes are sticky, dry, and may be coated with fibrin. 
The mucous membrane of the stomach and intestines may 
appear normal or sodden and oedematous, or may show 
traces of catarrhal inflammation. There may be croupous 
colitis. The intestinal glands are usually swollen. The 
intestines contain the rice-water discharge or a dark bloody 
fluid. The liver is anaemic; its cells may show parenchym¬ 
atous degeneration. The kidney is the seat of an acute de¬ 
generation which is well marked. The spleen, as a rule, 
is not enlarged. The lungs are collapsed, and may be con¬ 
gested at the bases. 

In patients who die in the stage of reaction the tissues 
are not so dry. The inflammatory changes in the lungs, 
stomach, and intestines, and the degeneration of the liver 
and kidneys, are more evident. 

Incubation is usually between two and three days. 

Symptoms.—The disease is usually described as occur¬ 
ring in the following five stages, although any of these 


CHOLERA. 


I 29 


stages may be omitted: 1. Stage of preliminary diarrhoea; 
2. Stage of purging; 3. Stage of collapse; 4. Stage of 
warmth; and 5. Stage of reaction. 

1. Stage of Preliminary Diarrhoea .—There is a diarrhoea 
with copious stools, attended with prostration and usually 
with nausea and vomiting. The stools are as dangerous in 
spreading the disease as those of the later stages. It is im¬ 
portant to recognize these cases early, as they are frequently 
amenable to treatment if it be not too long delayed. This 
diarrhoea may continue for from one to five days, and may 
either end in recovery or may pass into the second stage. 

2. Stage of Purging .—With or without this stage of pre¬ 
liminary diarrhoea the second stage begins abruptly, usually 
at night. The first symptom is copious purging, first of 
fecal passages, then of a frothy serous fluid without odor, 
containing whitish flakes of desquamated intestinal epithe¬ 
lium, to which appearance the name “ rice-water ” is applied. 
In some cases the discharges may be stained by blood. 
They may be accompanied by pain and griping, but usually 
their passage is painless, the fluid being voided in gushes or 
in an almost continuous stream. 

In rapidly fatal cases the patient may die before any purg¬ 
ing occurs. To these cases the term “ cholera sicca ” has 
been applied. Post-mortem examination shows the intes¬ 
tines to be full of the discharge, which has not been voided 
by reason of paralysis of the intestinal wall. 

Vomiting regularly follows the onset of purging, the 
vomited matters consisting of the stomach-contents, and 
later of the “ rice-water ” fluid. There are rapidly-developed 
symptoms due to the loss of water from the system. There 
is rapid emaciation; the skin is loose and wrinkled; the 
eyes are sunken ; the tongue is dry. The urine is dimin¬ 
ished, and contains urea in excess, albumin, and casts; it 
may be suppressed. There is distressing thirst, but whatever 
9 


I30 MANUAL OF THE PRACTICE OF MEDICINE. 

drink is taken is immediately rejected by the stomach. 
There are in the abdomen and legs muscular cramps which 
are often agonizing. The pulse becomes rapid and feeble; 
respirations are shallow and sighing. The skin is cold and 
clammy, but the internal temperature is elevated. The mind 
is anxious and distressed, but is unclouded. This stage 
lasts for from two to sixteen hours, and from it the patients 
may recover or may pass into the third stage. 

3. Stage of Collapse , or Algid Stage , or Cholera Asphyxia. 
—The vomiting and purging continue but become less pro¬ 
fuse, and may finally cease. The symptoms of collapse and 
heart failure increase rapidly. The skin is cold and 
shrunken and of a leaden hue; the pulse is more rapid and 
thready, becoming finally imperceptible. The external 
temperature is low; the internal temperature is somewhat 
elevated. This stage lasts for several hours or it may be 
protracted for a day or so, and it is apt to be fatal, although 
patients may pass into the warm stage, and die in that, or 
into the stage of reaction, and recover. 

4. Warm or Tepid Stage. —This stage is sometimes ob¬ 
served following the stage of collapse in patients about to 
die. The internal temperature rises; the skin becomes 
warm and of a more natural color. The purging and vomit¬ 
ing cease. The radial pulse can again be felt. The patient, 
however, becomes comatose, the urine is suppressed, and 
complicating inflammations of the pia mater, lungs, stomach, 
or intestines, or multiple abscesses, may develop. This 
stage is almost certainly fatal. 

5. Stage of Reaction. —The patient may pass into this 
from any stage of the disease, though but rarely from the 
stage of warmth. The symptoms rapidly disappear, and 
convalescence becomes established unless interrupted by 
complications. There may be seen a mottling of the skin 
or an erythematous rash. 


CHOLERA. 


131 

Complications and Sequelae.—There is frequently sup¬ 
pression of urine that may persist during the stage of reac¬ 
tion. The patient becomes delirious, the pulse becomes 
rapid and feeble, and death occurs with coma. To these 
cases the term “ cholera typhoid ” has been applied. The 
same symptoms may be produced by septic absorption by 
the denuded intestinal surface. 

Convalescence may be protracted by the continuance of 
gastro-enteritis, shown by irritability of stomach, pain, and 
diarrhoea. If croupous colitis occurs, it is apt to be fatal. 
There may be broncho-pneumonia or an irregular form of 
lobar pneumonia. There may be inflammation of any of 
the serous membranes in the long-continued cases. No 
symptoms, as a rule, result, and the occurrence of the 
lesion is known only from post-mortem evidence. There 
may be multiple abscesses or furuncles, frequently involving 
the parotid glands. There may be a continuance of the 
muscular spasms. 

“ Cholerine ” is a term frequently employed by French and 
German authors. By French writers it is applied to cases 
of the preliminary diarrhoea, by German writers it designates 
cases of cholera running a mild course and terminating in 
recovery. 

The prognosis varies from 20 to 80 per cent, according 
to the epidemic. The cases with preliminary diarrhoea 
most usually recover, especially if treated early. The prog¬ 
nosis in the stage of collapse is bad ; in the tepid stage, 
almost hopeless. 

Treatment.— Prophylaxis .—Entrance of imported cases 
into a port should be prevented by rigid quarantine. All 
merchandise and fomites should be steamed thoroughly. 
If quarantine and the disinfection of imported articles can 
be enforced thoroughly, spread of the disease should not 


occur. 


132 MANUAL OF THE PRACTICE OF MEDICINE. 

All discharges from cholera patients should be disin¬ 
fected, and all contamination of drinking-water scrupu¬ 
lously avoided. Those in attendance on the sick should 
wash the hands frequently in an acid disinfectant solution. 

Health inspectors should visit the poorer paits of the in¬ 
fected cities to stop any cases of diarrhoea and to treat all 
dieestive disturbances that may occur. All water should 
be boiled betore use. 

Attempts to procure immunity in man have not yet been 
successful. 

Medicinal Treatment .—Cases of preliminary diarrhoea 
should be treated promptly by regulation of the diet and 
by the use of astringents combined with opium. As the 
bacillus is killed by acids, any of the mineral acids may be 
given; salol also is recommended. The patient should 
be kept quiet and cool. When the disease has once devel¬ 
oped, treatment is directed toward mitigating the symptoms 
and preventing collapse. Warm applications and turpen¬ 
tine stupes to the abdomen and extiemities, and hot baths, 
are frequently grateful. 

The vomiting and purging are best treated by hypo¬ 
dermic injections of morphine, large doses being usually 
borne well. Calomel in a single dose of 20 grains placed 
drv on the tongue has at times been useiul. 

The thirst may be relieved by cracked ice, champagne, or 

acidulated water. 

Mineral acids and intestinal disinfectants, such as salol, 
salicylate of bismuth, and ^ 9 -naphthol, should theoretically 
be of service, but their administration is difficult because of 
the vomiting. 

To combat the dryness of the tissues and the concentra¬ 
tion of the blood, subcutaneous or intravenous injections of 
warm sterilized saline solutions should be employed, and 
they are often of the utmost value. Rectal injections may 


YELLOW EE FEE. 


133 


also be given when the purging is subsiding. Cantani 
recommends during the disease frequent high rectal injec¬ 
tions of the following solution, with the hips elevated : 


fy. Tannic acid, 



Laudanum, 

Water, 


Oij. 


The treatment by copious rectal enemata is termed “ enter- 
oclysis.” 

Heart failure is to be treated by hot applications and by 
hypodermic stimulation by ether, strychnine, digitalis, or 
whiskey. Inhalations of ammonia, amyl nitrite, or pure 
oxygen may be employed. 

During convalescence diuretics may be indicated. The 
diet should be regulated, and residual gastro-intestinal symp¬ 
toms should be treated as they may arise. 


YELLOW FEVER. 


Definition.—Yellow fever is an acute infectious disease; 
endemic in certain warm climates, and characterized by 
fever, jaundice, and a tendency to hemorrhages. 

Etiology.—The disease is endemic in certain localities, 
principally in the West Indian Islands, parts of the coast 
of the Gulf of Mexico, and the west coast of Africa. It 
is unknown in Europe. From time to time it makes epi¬ 
demic excursions into warm surrounding countries, and 
especially into the Southern United States. It may pene¬ 
trate into more northern cities to a slight degree in the sum¬ 
mer months. The epidemics are favored by poor hygiene 
and the crowding together of people and by a temperature of 
over yo° F. Lower temperatures diminish, and frost stops, 
the epidemic. Epidemics are more common on the sea- 
coast and in low altitudes, an elevation of one thousand 



134 MANUAL OF THE PRACTICE OF MEDICINE. 

feet procuring nearly absolute safety. I he spread of the 
disease is often checked by houses, walls, or streams. 

Immunity may be secured by a previous attack or by 
long residence in an endemic locality. Native races, tor the 
latter reason, are less liable to the disease, and when they 
are attacked the disease in them runs a mild course. 

Yellow fever is not contagious by contact with either the 
living or the dead body, but the germ is cast off, in some un¬ 
known way, in an immature state, and requires further devel¬ 
opment, after which infection can occur through the medium 
of the air or by fomites. The disease is introduced into 
cities chiefly by freight and merchandise, and quarantine 
and disinfection are successful if thoroughly performed. 

The specific germ has not yet been determined defi¬ 
nitely. 

Pathology. —The tissues of the body are usually in¬ 
tensely jaundiced. There may be subcutaneous hemor¬ 
rhages. The heart-muscle is pale and degenerated. The 
liver shows advanced fatty degeneration of its cells and is 
of a “ cafe au lait ” color. The spleen is not enlarged. The 
kidneys show the lesions of either acute diffuse inflamma¬ 
tion or a severe form of parenchymatous degeneration. The 
mucous membrane of the stomach is swollen and shows 
traces of a catarrhal inflammation, and there is frequently 
found in the stomach the “ black vomit,” which consists of 
mucus and altered blood. 

Incubation varies from one to twenty-five days, the aver¬ 
age duration being seven days ; it is less than this in severe 
cases. 

Symptoms.—The disease consists in severe cases of three 
stages: (i) stage of invasion; (2) stage of remission or 
“ stage of calm(3) stage of relapse. 

Stage of Invasion .—The onset is sudden and is initiated 
by a chill, or by convulsions in the case of children. The 


YELLOW EE FEE. 


135 


temperature rises rapidly to 103° F. in very mild cases, to 
105° or 106 0 F. in the severer forms, and it may be even 
higher. The pulse is usually full and ranges from 80 to 120, 
being usually less than would be expected from the height of 
the fever. In some cases the pulse is slowed from the first 
(50 to 60). Headache and pains in the back and in the 
bones are decided and severe; the face is flushed ; the eyes 
are suffused and watery. The stomach is irritable; sharp 
attacks of vomiting occur frequently, and may be of the 
projectile type. There may be vomiting of blood. The 
bowels are constipated. There are restlessness and possibly 
delirium or active mania. The urine is diminished and 
contains albumin and casts. 

While this is the usual course, mild cases are frequently 
seen. The patient may be walking about with a little fever 
(ioi° to 102° F.), headache, lassitude, and occasionally 
vomiting. The first stage usually lasts for three days, 
though it may terminate in from one to six days. 

The second stage , or the stage of calm, is marked by a fall 
of temperature, frequently to subnormal, and by disappear¬ 
ance of the other symptoms. In mild cases convalescence 
begins at this time. In these cases, as there is no jaundice, 
the term ‘'yellow” fever is evidently a misnomer. In some 
patients who recover, however, slight jaundice may appear 
on the fifth day. In severer cases, after the stage of calm 
has lasted for two days the patient develops the symptoms 
of the third stage. 

The third stage is marked by jaundice, by a tendency to 
hemorrhages, and usually by uraemic symptoms. The 
temperature rises, and the symptoms become aggravated. 
The pulse is gaseous and may be abnormally slow, falling 
sometimes to 40 beats in the minute. Jaundice now appears, 
of haematogenous origin, and is most pronounced. Vomiting 
begins anew, and in a considerable number of cases the so- 


136 MANUAL OF THE PRACTICE OF MEDICINE. 

called “black vomit” occurs. This is not always vomited, but 
may be retained in the stomach, there are usually hemor¬ 
rhages under the skin, forming large ecchymoses, and from 
any of the mucous membranes. Cerebral symptoms are 
usually present. The patient may become dull and stupid, 
or there may be delirium, frequently of the maniacal type. 
Fatal cases usually pass into coma. The urine, which is 
greatly diminished, contains large amounts of albumin and 
casts, and may contain blood; in severer cases it is alto¬ 
gether suppressed. 

In this stage the majority of patients die, from collapse, 
from the hemorrhages, or in a “ typhoid ” condition. In 
some cases death is due to uraemia. Fatal cases usually die 
between the fifth and the seventh day of the disease. 

Complications and sequelae are infrequent. There may 
be parotiditis, furunculosis, gastritis, or diarrhoea. 

Diagnosis.—The disease is chiefly to be diagnosed from 
malarial fever with complicating jaundice. These cases also 
frequently show a tendency to hemorrhage, and occur in the 
same locality and at the same time at which yellow fever is 
apt to appear. The presence of the malarial organism and 
the results of quinine treatment clear the diagnosis in doubt¬ 
ful cases. 

The prognosis depends upon the nature of the epidemic, 
varying from 10 to 85 per cent. It is better in private prac¬ 
tice and among the native races and in young, temperate 
individuals. Cerebral symptoms, hemorrhages, suppression 
of urine, and pronounced jaundice mark the bad cases. 

Treatment.— Prophylaxis .—There should be rigorous dis¬ 
infection of all ships, merchandise, and mails arriving from 
infected localities. Patients should be quarantined abso¬ 
lutely, and their clothing and bedding be disinfected. In 
infected localities persons who are not necessary for the care 
of the sick should not remain. 


SYPHILIS. 


137 


The patient should be nursed carefully in a well-ventilated 
room, and symptoms should be treated as they arise. 

Diaphoresis in the first stage often affords relief, while the 
headache and pains are best controlled by phenacetine, salol, 
opium, or single large doses of quinine. 

The fever, if high, may be reduced by cold baths, spong¬ 
ing, the cold pack, or internal antipyretics. 

Vomiting is controlled by sinapisms, dilute hydrocyanic 
acid, oxalate of cerium, cocaine in gr. jr doses, cracked ice, 
bismuth, or by rest and by hypodermatics of morphine. 

Internal styptics have but little control over the hemor¬ 
rhages. 

Suppression of urine is to be treated by cups and poultices 
applied to the kidneys, diuretics, rectal injections of warm salt 
water, or the hot steam bath. Sternberg recommends small 
doses of bichloride of mercury with bicarbonate of soda. 

The action of the heart is to be sustained by stimulants 
given in sufficient doses to avert danger from collapse. 

SYPHILIS. 

Syphilis occurs in all civilized countries, and all races are 
susceptible. Among aboriginal races it becomes a formid¬ 
able disease, but modern methods of treatment have greatly 
reduced its virulence. It is said to have been inoculated 
in monkeys and apes, but it is doubtful if it exists in other 
lower animals. Synonym : The pox. 

Lustgarten in 1844 described a bacillus somewhat shorter 
than the tubercle bacillus, not occurring free, but in the cells, 
and found in the secretions of syphilitic sores and in some 
gummata and condylomata. It is almost identical in appear¬ 
ance with the smegma bacillus. The causative relation of 
this bacillus to the disease has not yet been absolutely 
proven. Syphilis may occur as an acquired and as a 
hereditary disease. 


138 MANUAL OF THE PRACTICE OF MEDICINE. 


Acquired Syphilis. 

Acquired syphilis, which is the most usual form, is due to 
inoculation by the discharges from the earlier lesions of the 
disease. Ordinarily it results from sexual intercourse, through 
minute abrasions of the genitalia. “ Extra-genital syphilis 
may be caused by infected throat or dental instruments, 
razors, pipes, cigars, cups, eating utensils, and by kissing or 
by beastly practices. It may be caused by infected human¬ 
ized virus in vaccination, or by wet-nurses. It is not trans¬ 
mitted through normal secretions. Once acquired, it is rare 
that the disease can be reinoculated successfully. 

Periods of the Disease. —Three periods are described . 
(1) A primary stage, from the moment of infection until 
the outbreak of constitutional symptoms, lasting for eight 
to ten weeks. There are two sub-periods to this stage . (tf) 
first incubation period of from fourteen to twenty-one days, 
terminating with the appearance of the primary sore ; (b) 
second incubation period, lasting from the appearance of 
the primary sore until the outbreak of the constitutional 
symptoms. (2) A secondary stage, comprising the fever, 
exanthemata, and their complications, lasting from one to 
three years. (3) A tertiary stage, consisting of gummata, 

visceral syphilis, and sequelae. 

Symptoms of the Primary Stage. —The first incubation 
period lasts for from fourteen to twenty-one days after infec¬ 
tion, without symptoms. 

The second incubation period is initiated by the develop¬ 
ment of the chancre (“ hard,” “ indurated,” or “ Hunterian ” 
chancre), which begins as a red papule on an indurated base, 
grows for from two to four weeks, and then slowly ulcerates 
in the centre; or it may begin as an indurated, indolent sore. 
Suppuration and gangrene may occur as secondary processes 
in weakly and alcoholic subjects. The chancre appears as 


SYPHILIS. 


139 


an indurated papule on the preputial sulcus, in the orifice 
of the urethra, on the edge of the labia, or on the lips. 
The induration is broad and shallow (“ parchment indura¬ 
tion ”) upon the glans penis and on the inner surface of the 
labia. There is but one chancre, with but rare exceptions. 

Care should be taken not to mistake the inflammatory 
induration following caustic applications to chancroids or 
herpes for that of a true chancre, and the possibility of a 
mixed infection of chancre and chancroid must be borne 
in mind. Microscopically the chancre consists of a cellular 
infiltration with acute obliterating endarteritis of the neigh¬ 
boring arteries. 

Painless swelling of the neighboring lymph-glands occurs 
from eight to fourteen days after the appearance of the 
chancre, the glands all over the body becoming affected, 
the nearest glands being enlarged first. Thus in genital 
syphilis the inguinal glands become enlarged in the third 
or fourth week after the original infection, the axillary glands 
in the fifth week, and the cervical glands in the seventh 
week. The lymphatics entering the glands may be felt 
often as indurated cords. Suppuration does not occur 
unless from some secondary pus infection. 

Symptoms of the Secondary Stage. —There may be fever 
ushering in the second stage, or the fever may appear late in 
the disease. The temperature may be 101 0 to 103° F., or even 
104° to 105 0 F. It is marked by remissions, and, as a rule, 
persists for but a few days. Exceptionally the fever may 
last for weeks or months, and a diagnosis from malarial fever 
may be difficult. In one case observed by the writer the 
fever lasted for over four months, notwithstanding energetic 
antisyphilitic treatment. The spleen in prolonged fever cases 
is enlarged. Pharyngitis with a sharp line of demarcation 
on the soft palate, and tonsillitis with superficial symmetrical 
ulceration, are often noted, usually at the time of fever, and 


140 MANUAL OF THE PRACTICE OF MEDICINE. 

headache, lassitude, and pains in the back and in the limbs 
are complained of. 

A macular eruption usually manifests itself as the first 
eruption. It appears on the abdomen during the eighth 
week after infection; on the chest during the ninth week; 
on the shoulders during the tenth week; on the arms 
during the eleventh week; on the forearms during the 
twelfth week; and on the hands during the thirteenth week. 
This eruption is symmetrical, follows the cleft-lines of 
the skin, and is of a dull coppery color. Papules occur 
somewhat later, being rarely seen before the third month 
after infection. They may be small or large, occurring 
in a row below the line of the hair on the forehead; they 
constitute the corona Venerea. Pustules may occur as a 
late exanthem rarely before the fourth month. The pus¬ 
tules may be small and shotty, closely resembling variola, 
or they maybe large like impetigo, or they may be changed 
into deep ulcerations covered by rupial crusts. 

A squamous form of eruption is described, not unlike 
psoriasis, but less scaly. This form usually is seen on the 
palms of the hands and the soles of the feet. 

If papules occur in regions where the skin is moist, as 
about the anus and vulva, they become sodden, devoid of 
epidermis, and show white points upon their surface. These 
papules are the “ flat condylomata.'’ 

The eruptions appearing in mucous membranes undergo 
maceration and are known as mucous patches, warts, and 
condylomata. 

Mucous patches are rounded, slightly raised, and covered 
with a grayish film. Their discharge is exceedingly virulent. 
They are usually seen on the inner side of the cheek, oppo¬ 
site the second molar tooth, on the under surface of the 
tongue, and at the angles of the mouth. They are really 
macerated syphilitic papules. If the papillae in the papule 


SYPHILIS. 


141 

hypertrophy, they constitute the condyloma or wart, accord¬ 
ing to whether or not the papules are fused. 

For a detailed description of syphilitic eruptions the 
reader is referred to special works on dermatology. 

There may be extensive thinning of the hair. Iritis may 
develop in from three to six months after the chancre, and 
may be serious. Anaemia and cachexia may be marked dur¬ 
ing the secondary stage, which lasts for from one to three years. 

Symptoms of the Tertiary Stage. —This stage is marked 
by late syphilides, gummata, amyloid degeneration, sclerosis, 
and visceral disease. 

Late syphilides are unsymmetrical and have a tendency 
to deep ulceration, leaving cicatrices. The rupial stratified 
crusts cover round deep ulcers. Periosteal nodes along the 
course of the tibiae are commonly observed. Syphilitic 
periostitis is marked by severe pain, worse at night—the so- 
called “ osteocopic pain.” Tubercular and unsymmetrical 
serpiginous eruptions characterize the tertiary period. 

Gummata may develop in the skin, the subcutaneous 
tissues, the muscles, or the internal organs. They may be 
distinctly circumscribed, or they may occur as a diffused 
infiltration. The nodule or gumma consists of small cells 
with a gelatinous basement substance. It may remain un¬ 
changed, may become absorbed, may undergo cheesy degen¬ 
eration can be invested with a fibrous capsule, may be con¬ 
verted to fibrous tissue, or may suppurate. Gummata of the 
skin, of the mucous membranes, of the bones, and of the 
cartilages undergo ulceration and extensive sloughing. In 
this way the cartilages of the nose may disappear, or there 
may be an ozaena with necrosed bone in the nose, or the 
palate or the tonsils maybe totally ulcerated. Cicatrices of 
the mucous membranes may result in stricture. 

In the viscera gummata frequently undergo fibroid trans¬ 
formation with puckering and deformity. 


142 MANUAL OF THE PRACTICE OF MEDICINE. 

Amyloid degeneration frequently follows tertiary syphilis, 
and degeneration-changes of a sclerotic nature are com¬ 
monly observed, as in locomotor ataxia and arterio-sclerosis. 

The internal forms of syphilis will be treated of in detail 
under the titles of the diseases of the various organs. 

It is important to remember that the division into the 
three stages is not always sharply drawn in actual experi¬ 
ence, symptoms of one stage overlapping and encroaching 
upon those of the preceding or the following period ; it 
should be borne in mind also that by systematic judicious 
treatment the course of the disease can be modified materi¬ 
ally. There are also light cases in which tertiary and even 
secondary symptoms may not develop, especially if the case 
be treated from the start. 

The disease is not considered inoculable after the third 
year. 

The prognosis is generally good. Visceral sy^philis, 
especially of the brain and its membranes, may terminate 
fatally, or death may indirectly result by arterio-sclerosis, 
aneurysm, or locomotor ataxia. 

Treatment.— Prophylactic .—Syphilitic patients should not 
marry until three years have elapsed since the infection. It 
is even better to extend this period to five years. Personal 
prophylaxis consists in personal purity. Governmental reg¬ 
ulation of prostitution hardly lessens the dangers. Surgical 
and dental instruments should be sterilized scrupulously, 
and it is better for the surgeon to have two sets of instru¬ 
ments, one set being used exclusively for syphilitic patients. 
Surgeons should handle syphilitic lesions with care, espe¬ 
cially if there be abrasions on the fingers, and after such 
handling should cleanse their hands in strong antiseptic 
solutions. Syphilitic patients with mucous patches should 
have their own drinking and eating utensils and their own 
towels, and should be prohibited from kissing. A syphilitic 


SYPHILIS. 


143 


husband should live apart from his wife for at least two 
years. 

Curative. — (a) Treatment of the Primary Stage .—It is of 
no use to excise the chancre. No regular treatment should 
be initiated until the macular eruption appears, making the 
diagnosis positive. Should sloughing or suppuration occur, 
it should be treated on general principles. 

(/;) Treatment of the Secondary Stage .—The specific drug 
is mercury. Its use should be begun upon the first appear¬ 
ance of the macular eruption, and be continued for at least 
two years—for the first year alone, and for the second year 
combined with iodide of potassium. 

There are two ways of giving mercury: One way is to 
give it intermittently, whenever symptoms appear, ceasing 
its use in quiescent periods; the other way is to give it 
steadily in small tonic doses. The latter plan seems pre¬ 
ferable. 

Mercury may be given in the following ways: Gray 
powder, or hydrargyrum cum creta, gr. j, with gr. j of 
Dover’s powder, in pill, four to six times a day; tab¬ 
lets of the biniodide, gr. y 1 ^, three times a day; tablets 
of the protiodide, gr. I, three times a day. Inunctions 
of mercurial ointment may be used. One dram suffices 
for a single inunction, and one application a day suf¬ 
fices. The ointment should be rubbed on successive 
nights into the lateral aspects of the thorax and the arm 
on one and then on the other side, then on the sides of the 
abdomen, then on the inner side of either thigh. This 
gives six localities for application. At the end of six days 
the patient should take a hot bath, and then the circuit is 
again gone over. Mercurial inunctions are recommended 
when an immediate effect is desired. 

Subcutaneous injections of mercury have been recom¬ 
mended warmly. With a sterilized needle the bichloride 


144 MANUAL OF THE PRACTICE OF MEDICINE . 


(gr. ^ in Tllxx of water) or calomel (gr. j-ij in Tflxx of 
glycerin or of olive oil) may be injected once a week into 
the gluteal region. Such injections, however, are apt to 
be painful. 

Fumigations of calomel may be employed, the patient 
sitting in a chair wrapped in a blanket. Under the chair is 
to be placed an alcohol lamp over which is a strip of tin 
properly supported in place, 20 grains of calomel being piled 
in a heap at the point where the flame touches the tin 
(Fig. 1). The patient goes to bed after the fumigation, 
still wrapped in the blanket. 

During the mercurial treatment care should be taken not 
to push the drug to the point of salivation. Before the 
treatment the teeth should be put in order and the tartar be 
removed. During the treatment the teeth should be 
brushed twice a day, and gargles of a saturated solution of 
chlorate of potassium be ordered. Green vegetables and 
fruit should be avoided. Upon the first appearance of sali¬ 
vation the drug should be stopped for the time. Should 
diarrhcea follow the internal use of mercurials, small doses 
of Dover’s powder or of opium should be given in com¬ 
bination. Anaemic conditions call for the simultaneous 
administration of iron, and proper hygiene must be en¬ 
forced in every instance. 

At the close of one year there seems to be an advantage 
in combining potassium iodide with the mercury (“ mixed 
treatment ”), as in the following prescriptions : 

R. Hydrarg. bichloridi, gr. j; 

Potassii iodidi, 3v; 

Aquae, 

Syr. sarsaparillae comp., aa sij.—M. 

Sig. A teaspoonful, largely diluted, after each meal. 


SYPHILIS. 


M5 


It. Hydrarg. bichloridi, 
Potassii iodidi, 

Tinct. cinchon. comp., 
Aquae, 



Sig. A teaspoonful in water after each meal. 

(f) Treatment of the Tertiary Stage. —The drug par excel¬ 
lence is iodide of potassium, which has a specific action. 
The initial dose is from io to 30 grains three times a day, 
largely diluted in water or in milk. In certain cases the 
drug should be pushed to greater limits, from 3 to 4 drams 
being required for a single dose. This is especially the 
case in cerebral syphilis. 


Hereditary Syphilis. 


The hereditary differs from the acquired form of syphilis 
chiefly in the absence of the primary stage. 

Etiology.— Father Syphilitic. — (a) The child may be 
infected directly (sperm inheritance). The nearer the pro¬ 
creation is to the primary lesion in the father, the greater 
are the chances of the child being infected. The power of 
transmission rarely exceeds three or four years. It is 
possible, however, for a syphilitic father to beget a healthy 
child. (b) The mother may be infected through the 
placental circulation, but, whether or not active syphilis 
appears, a syphilitic child cannot infect the mother after 
birth, a maternal immunity having been created. This is 
known as Colies’ law. 

Mother Syphilitic. —If the mother be in the active stages 
at the time of conception, the embryo is usually infected. 
If the disease be acquired a few months prior to labor, the 
child usually escapes. Infection of the child may be min¬ 
imized by judicious antisyphilitic treatment of the mother 
during pregnancy. About one-third of mothers abort, and 


10 


146 MANUAL OF THE PRACTICE OF MEDICINE. 

gummatous placenta or degeneration of the placental folli¬ 
cles may be found. 

Both Parents Syphilitic .—The infant mortality from pater¬ 
nal transmission is 28 per cent.; from maternal transmission 
60 per cent.; from both mother and father, 68 per cent. 
Parents with tertiary syphilis are apt to beget sickly 
children with a tendency to neurotic affections. 

Symptoms.—If the child be born diseased, there is evi¬ 
dent poor development and malnutrition. Bullae (pemphi¬ 
gus neonatorum) are usually seen upon the hands and feet; 
the lips are fissured; the child snuffles; the liver and spleen 
are enlarged; and the epiphyses are apt to be separated. 
Such a child is not likely to survive. 

If the child be born apparently healthy, symptoms may 
not develop until the fourth to the eighth week. Then the 
child snuffles and cutaneous lesions are apt to appear, 
especially about the nates. There are usually brownish- 
red patches with a well-defined border, or they may be 
papular. Indolent boils in a copper-colored base may 
develop. Fissures (rhagades) are apt to develop about the 
lips, the secretions from such fissures being intensely viru¬ 
lent. The resulting cicatrices are characteristic. There 
may be falling out of the hair. Syphilitic onychia may 
develop. 

General glandular enlargements are not so common in the 
hereditary as in the acquired form of syphilis. There may 
be purpura haemorrhagica neonatorum, associated usually 
with diseased arteries. The child is apt to show increasing 
malnutrition, looking like a wrinkled old man. The cry is 
shrill and piercing. Various cutaneous eruptions may 
appear, with mucous patches or with ulcerations of mucous 
membranes. The nose may fall in. Developmental lesions 
of bones may develop. There may be thinning of the 
bones of the skull (craniotabes) or irregular growth of 


SYPHILIS. 


H7 


bone. There may be separation or suppuration of the 
epiphyseal ends of bones, or formation of osteophytes on 
the long bones. There may be gummata of internal viscera. 

The teeth are apt to be deformed, constituting the 
“Hutchinson teeth” (PL io, Fig. 2). The upper central 
incisors of the permanent set are usually the ones most 
involved. The teeth are peg-shaped, stunted, and at the 
cutting edge there is a notch in which the dentine is ex¬ 
posed. 

Interstitial keratitis is apt to occur about puberty. The 
cornea has a ground-glass appearance which may disappear 
or may lead to permanent opacity. There may be iritis. 
Deafness from labyrinthine disease may develop. The patient 
has a generally stunted appearance—undersized, and appar¬ 
ently much younger than he really is. There may be 
nodosities of the long bones from gummatous periostitis, 
or there may be dactylitis. For a detailed account of 
joint- and bone-lesions the reader is referred to works on 
surgery. 

Treatment.—The mother should receive mixed treat¬ 
ment throughout pregnancy, and the treatment should be 
continued with the child. The treatment of the child is 
like that of adults, but proportionately smaller doses should 
be given. 

The syrup of Giberts is recommended: 

Hydrarg. biniodidi, gr. ss ; 

Potassii iodidi, 3ij; 

Syr. zingiberis, 

Aq. destillat., aa 31J. —M. 

Sig. Dose, gtt. v-x for a child six months old. 

As a rule, mercurials have less effect upon the gums and 
more effect upon the bowels in children than in adults. 


148 MANUAL OF THE PRACTICE OF MEDICINE. 


ACUTE MILIARY TUBERCULOSIS. 

Definition. —Acute miliary tuberculosis is an acute 
tubercular infection characterized by an eruption of miliary 
tubercles in various parts of the body, with fever, symptoms 
of local infection, and a fatal ending. 

Etiology. —The etiology of tubercular disease is con¬ 
sidered in detail under Tubercular Disease of the Lungs 
(p. 373). Miliary tuberculosis is a general infection follow¬ 
ing some local tubercular lesion, and is due to the escape 
of tubercle bacilli into the blood, where they find lodgement 
in various organs and develop tubercles. 

The primary tubercular focus may be apparent or may 
be unsuspected. It may be local tubercular disease of the 
lung, of the lymph-glands, of the kidneys, or of the bones. 
Frequently the source is found to be tubercular bronchial 
glands, which may even rupture into a pulmonary vein and 
shower bacilli into the circulation. A primary tuberculosis 
of the thoracic duct has been demonstrated. Well-marked 
cases of miliary tuberculosis have followed the use of 
Koch’s tuberculin given for the cure of a local tubercular 
inflammation. 

Pathology. —Tubercles (for the detailed structure of 
which see Tubercular Disease of the Lungs) are found in 
various organs of the body. They are usually the size of a 
pin’s head, but they may appear larger from a number 
being coalesced. When recent they are translucent, gray¬ 
ish, and contain bacilli. In older cases they may be 
caseous and yellow in the centre and may contain no 
bacilli. Tubercles may be found in the lungs, pleura, peri¬ 
toneum, liver, kidneys, lymph-glands, pia mater, in the 
bone-marrow, and in the choroid coat of the eye. Less 
frequently they are found in other parts. There is no 
regularity about their distribution : they may be abundant 


ACUTE MILIARY TUBERCULOSIS. 


149 


in some organs and scanty or absent in others, or they may 
be more generally distributed. This lack of regularity 
gives rise to great variations in clinical types. With the 
tubercles are often found associated various forms of in¬ 
flammatory products or ordinary granulation-tissue. 

Symptoms are general and local. 

General symptoms are due to toxines of the general infec¬ 
tion. Fever is a marked feature and lasts throughout the 
disease. Its absence is rare. It may be intermittent at the 
onset, resembling malarial fever. At the height of the 
disease it is usually markedly remittent, though it may be 
continuous. An “ inversive type ” has been described in 
which the highest temperature occurs in the morning—a 
peculiarity rarely seen in other diseases. 

The pulse is more rapid and feeble than can be accounted 
for by the fever, running between no and 130. 

The breathing is rapid, sometimes as frequent as 40 to 60 
to the minute, and it is characteristic for the patient not 
to complain of shortness of the breath. 

There may be profuse sweats. These may occur after 
remissions of temperature, or irregularly as an evidence of 
sepsis. 

The mental condition is usually cheerful, and the mind is 
bright even in long-continued cases; the patient complains 
only of “ having fever and a little cold.” This sign is highly 
characteristic, and is often a good point of diagnosis from 
typhoid fever. 

In acute cases with meningitis there may be delirium 
which is either mild or severe and amounting to mania. 
Stupor or coma succeeds the delirium. 

The spleen is usually large; the urine is that of fever, or 
it may contain albumin. 

The close of the disease is characterized by the symptoms 
of the typhoid state. 


150 MANUAL OF THE PRACTICE OF MEDICINE. 

Local symptoms depend upon the locality and extent of 
the tubercular deposits in the various viscera. While many 
organs are invaded, some are more apt to give symptoms 
than others, and the organ most invaded will give a leading 
character to the local symptoms. 

If the meninges are involved, the local symptoms will be 
those of meningitis. It is important to remember that in 
children tubercular meningitis is acute miliary tuberculosis 
with symptoms of meningitis, while in adults it is possible 
for it to be a local lesion without involvement of other organs. 

Involvement of the pleura gives rise to pleurisy. A 
double pleurisy with effusion or a hemorrhagic effusion is 
highly characteristic. 

Involvement of the lungs can be described as occurring in 
three stages. There is first a fine bronchitis of the smallest 
tubes over both lungs, especially at the apices, and associated 
with dry pleurisy in patches. The physical signs are those 
of fine bronchitis and dry pleurisy. As the tubercles increase 
in number they coalesce, so that parts of the lungs, especially 
the apices, become consolidated, giving rise to areas of dul- 
ness, to bronchial voice and breathing, and to increased 
vocal fremitus. In the third stage the coalesced tubercles 
break down to form small cavities, so that the breathing be¬ 
comes broncho-cavernous and there are gurgles. The sub¬ 
jective symptoms consist of cough, rapid breathing, rarely 
a feeling of dyspnoea, slight cyanosis, and an expectoration 
of muco-pus sometimes admixed with blood and containing 
bacilli. 

Involvement of the peritoneum is shown by ascites, tym¬ 
panites, constipation, and sometimes by pain. In other 
cases there may be no symptoms although the peritoneum 
be extensively involved. 

Tubercles in the choroid can be detected by expert 
ophthalmologists. 


ACUTE MILIARY TUBERCULOSIS. 


Plate ii. 



Chart of acute general miliary tuberculosis : tubercles in the pia mater, pleurae, lungs, peritoneum, liver, kidneys, and intestines. “ Inversive temperature " during the eleventh and twelfth weeks 










































































































































































































































































































































































































































































































































































































































ACUTE MILIARY TUBERCULOSIS . I 5 1 

In all cases the diagnosis is made by adding the general 
to the local symptoms. In some cases the general outweigh 
the local symptoms, and the disease resembles malarial 
or typhoid fever. In other cases the local symptoms are 
the more prominent, and the cases resemble meningitis, 
pleurisy, broncho-pneumonia, or peritonitis. 

Types of the Disease. —1. Fever Type .—The disease be¬ 
gins like typhoid and runs for three or four weeks, with 
enlarged spleen. There are no hemorrhages and no spots; 
bronchitis is more marked, the pulse and breathing are more 
rapid, and the mind is clear. At the end of this time the 
patient may die, and the diagnosis may be difficult unless 
advancing lesions in the lungs and bacilli in the sputum can 
be demonstrated. Other cases go on for three or four 
months, with high remittent fever, developing areas of con¬ 
solidation and breaking down in the lungs, and die ex¬ 
hausted. In these cases the lungs are the seat of the chief 
deposits. Other cases run the same course, but we have 
in addition the local symptoms from other organs (see 
PI. n). In still other cases the temperature at the onset 
is intermittent, resembling malarial fever. 

2. Meningeal Type .—Here the picture is that of tubercular 
meningitis. The difference between tubercular meningitis 
in children and in adults has been alluded to. 

3. Mania or Delirium Type .—Acute mania or active talk¬ 
ative delirium may be the first symptom, associated with 
fever. Stupor and coma follow, and death results, usually 
within three weeks. 

4. Pulmonary Type .—There may be a pleurisy with fever 
out of proportion to the apparent lesion, or the disease may 
begin as a bronchitis or a broncho-pneumonia. Any bron¬ 
chitis which persists for some weeks, with high fever, rapid 
pulse, and respiration with fine rales heard especially at the 
apices, should be regarded with suspicion. 


152 MANUAL OF THE PRACTICE OF MEDICINE. 

5. Any of the preceding types may be complicated by 
symptoms of a pre-existing local tubercular lesion. 

Diagnosis is aided by the following characteristics: In 
most cases there is a previous tubercular lesion. There is 
evidence of a diffused disease, such as meningitis, double 
pleurisy, and bronchitis, in the same patient. Objective 
symptoms are more marked than are the subjective ones. 
The patient “ feels all right” and yet is evidently sick. In 
most cases bacilli can be demonstrated in the sputa and 
tubercles can be seen in the choroid. 

There is an advancing lesion in the lung, with diffused 
fine rales, both bronchial and pleural; later, consolidation 
and breaking down in small areas. 

In all cases the disease runs a progressively downward 
course and terminates fatally. Removal of pleuritic or 
ascitic accumulations is followed by a return of the effu¬ 
sion. 

Prognosis. —The disease is surely fatal. Some cases are 
fatal in from seven to ten days; more commonly they run 
for three or four weeks or as many months, and very rarely 
for a year. Meningeal cases are more rapid than the fever 
or .the pulmonary type. 

Treatment is entirely symptomatic. The patient is to be 
fed, nursed, and made comfortable. 

The sputa should be sterilized to prevent the spread of 
the disease. 


MALARIAL FEVER. 

Definition.—Malarial fever is a specific, non-contagious 
disease caused by the plasmodium malarias, and is character¬ 
ized by paroxysmal fever, enlargement of the spleen, and a 
tendency to extreme anaemia. 

Etiology. —The plasmodium malarias, discovered in 1880 


MALARIAL FEVER. 


153 


by Laveran in Algiers, is not a bacterium, but is a form of 
protozoon or haematozoon. Though it has not been culti¬ 
vated successfully, it is undoubtedly causative of the disease, 
and is of the utmost diagnostic value. It is found free in the 
blood and in the red blood-cells. The blood-cells become 
destroyed; their pigment is set free, and is found in black¬ 
ish granules in the plasmodia, in the white cells, in the 
endothelial cells of the capillaries, and in free granules and 
masses. Osier describes the following six forms: (1) An 
unpigmented hyaline body within the red corpuscles, dis¬ 
playing active movements; (2) a pigmented amoeboid body 
within the red corpuscles that may increase in size and 
form ; (3) a segmenting body in which the protoplasm 
divides into a number of definite small spheres; (4) cres¬ 
centic bodies which develop within the blood-corpuscles; 
(5) flagellate bodies; (6) the flagellae. 

The crescents are most constant in malarial cachexia. 
The flagellate bodies are usually found in the blood of the 
spleen, and they have no definite relation to any clinical 
form. The larger amoeboid and hyaline bodies are usually 
associated with the acuter forms, and are readily destroyed 
by quinine. The flagellate bodies are difficult to see unless 
in motion, hence they are searched for only in fresh blood. 
The other varieties can be found best by rapid drying, fixa¬ 
tion by artificial heat, with staining by a concentrated solu¬ 
tion of methyl-blue or of gentian-violet. 

The details of the life-history of the plasmodium are 
unknown. It is not known in what ways it enters or leaves 
the body, although it is supposed that infection may occur 
by inhaling malarial air or by drinking malarial water. 
The disease is not contagious. 

Conditions Favoring Infection.— Climate .—The disease 
is endemic in the tropics, being less common in the temper¬ 
ate zones. In the tropics it occurs in severe forms with a 


154 manual of the practice of medicine. 

large annual mortality. In temperate countries severe cases 
are rare unless they be imported. Mild cases occur often, 
appearing and disappearing in different years. 

Season .—In the tropics cases may develop at any time, 
especially after the rainy season. In temperate climates the 
disease is chiefly one of the summer and autumn. 

Age .—All ages are susceptible, but adults are more 
exposed to the miasm. 

Sex .—The disease is more common in men because of 
increased exposure. 

Race .—Strangers are more frequently affected than 
natives. Colored races are less susceptible than other races 
to the acute forms, but may suffer from malarial cachexia. 
Their immunity, however, is becoming less and less, and is 
often lost by a change of residence even to a non-malarial 
district. 

Altitude .—Malarial fever is usually a disease of low alti¬ 
tudes, but it has been found at high elevations. 

The soil is the breeding-place of the germ. Moisture, a 
temperature of 6o° F. and over, and decaying vegetable 
matter afford the best conditions for its development. Low- 
lying sea-marshes and the course of rivers entering them, 
fresh-water marshes, especially if stagnant or if tainted with 
brine, damp, poorly-drained soil, and soil broken for the first 
time or left to waste for a number of years after cultivation, 
are the favorite localities for the miasm. 

Degree of Exposure .—In temperate climates prolonged 
exposure is usually necessary; this is not the case in the 
tropics. Infection is more potent at night than during the 
day. The germ can be carried for great distances by wind 
blowing from infected localities. 

Pathology.—There are certain lesions common to all 
forms. There are pigment-granules, either free in the blood 
or in the plasmodia, the white cells, and the endothelium 


MALARIAL FEVER. 


155 


of the blood-vessels. The pigmentation of the blood-ves¬ 
sels is more marked in some viscera than in others, being 
especially marked in the liver, spleen, and brain. In bad 
cases all the organs are pigmented grayish brown or even 
black. 

The spleen in acute cases is congested, softened, and en¬ 
larged. It may rupture, causing fatal hemorrhage. There 
may be hemorrhagic infarctions in its substance. In pro¬ 
tracted cases the spleen is large and firm, constituting a true 
hypertrophy. 

The blood becomes anaemic from the destruction of the 
red cells. In protracted cases it may even resemble the 
blood of pernicious anaemia. 

The liver during an acute attack is often congested and 
enlarged. Malarial hepatitis and malarial pneumonia have 
been described, but their occurrence has not been estab¬ 
lished satisfactorily. The presence of the plasmodia has 
already been alluded to. 

Clinical Forms.—There are five clinical forms of malarial 
fever : 1. Intermittent fever; 2. Pernicious intermittent fever; 
3. Remittent fever; 4. Pernicious remittent fever; 5. Ma¬ 
larial cachexia. 

1. Intermittent Fever (Ague; Chills and fever).— Symp¬ 
toms .—There may be a period of incubation of from 
twenty-four hours to several months. The disease occurs 
in paroxysms, of which three stages are described. 

The cold stage is marked by a chill which is often severe 
and shaking. The skin is cold, but the internal tempera¬ 
ture is raised frequently to 105° or 106° F. The rise of 
temperature usually antedates the chill. There are severe 
headache, and frequently nausea and vomiting. The pulse 
is rapid. The urine is increased in quantity. This stage 
lasts for from half an hour to two hours. 

In the hot stage the skin becomes hot and flushed, and 


156 MANUAL OF THE PRACTICE OF MEDICINE. 

the fever, which may be between 102° and 107° F., becomes 
apparent. The pulse is full and bounding. There is a 
throbbing headache. There may be pains in the back and 
in the bones. There may be vomiting. The spleen is 
enlarged and tender on palpation. Examination of the 
blood reveals the organism. This stage lasts for from three 
to six hours. 

The sweating stage is marked by the subsidence of the 
fever to normal or subnormal and by profuse sweating. The 
headache is apt to persist for some hours after the paroxysm. 

The total duration of a paroxysm is between six and 
twelve hours. Between the paroxysms the temperature is 
normal and the patient complains only of lassitude. In pro¬ 
tracted cases, however, there may be developed hypertrophy 
of the spleen, anaemia, and malarial cachexia. The parox¬ 
ysms recur with striking periodicity, and according to the 
length of the intervals the principal types of malarial fever 
receive different names. In quotidian fever the interval is 
twenty-four hours, the paroxysm returning daily at the 
same hour. In tertian fever the interval is forty-eight hours, 
the paroxysm returning every other day at the same hour, 
which is every third day if the day of commencement of the 
fever be counted as the first day. In “ quartan ” fever the 
interval is seventy-two hours. Other forms are designated 
“ quintan,” “ sextan,” “ heptan,” and “ octan,” but they are 
of exceedingly rare occurrence. A “ double quotidian ” is 
a form in which two paroxysms occur in the twenty-four 
hours. In “ double tertian ” severe paroxysms occur every 
third day, with mild paroxysms on the intervening days. 

Exceptional Cases .—In mild cases the chill is frequently 
absent—the so-called “ dumb ague.” This form occurs in 
the older residents of a malarial locality. In other cases 
the sweating stage is absent, fever and headache being 
the most constant symptoms. 


MALARIAL FEVER. Plate 12. 



. 1 ertiary intermittent fever following 2. Tertian intermittent 3. Quotidian intermittent 

defervescence of lobar pneumonia. fever. fever 





























































































































































































































MALARIAL FEVER. Plate it 



Temperature chart of remittent fever. 










































































































































































MALARIAL FEVER. 157 

In long-continued cases the paroxysms become irregular 
and erratic as to both periodicity and severity. 

If malarial infection occurs during the course of other 
disease, it gives to the original fever a greater degree of 
remittency. 

In some patients a paroxysm may consist of a chill, 
fever, and the passage of urine stained with haemoglobin. 

2. Pernicious Intermittent Fever. —Cases of the pernicious 
form are but rarely seen in temperate climates unless they 
be imported from some intensely malarial locality. In the 
Northern cities of the United States cases commonly are 
brought from the Southern cities and from Panama. The 
disease is often called “ Panama fever ” or “ Chagres fever.” 
A number of types have been described: 

(1) Some cases resemble severe forms of ordinary inter¬ 
mittent fever. 

(2) Some patients pass from the paroxysm into a con¬ 
dition of coma or collapse in which they may die. If they 
recover, they are apt to die in the next paroxysm unless 
energetically treated by quinine. 

(3) Some patients pass during a paroxysm into active 
delirium or mania which may change into coma. 

(4) Some patients during the febrile paroxysm develop 
severe pulmonary symptoms , dyspnoea, cough, and expec¬ 
toration which may contain blood. Examination may 
reveal the physical signs of a pneumonic patch or of an 
area of pleurisy that disappears should the patient survive 
the paroxysm. 

(5) In other patients during the paroxysm there may be 
gastric or intestinal symptoms. There may be pain referred 
to the stomach, vomiting, and haematemesis. There may 
be purging resembling that of cholera, and the patient may 
pass blood from the bowel. 

(6) Some cases are marked by a disposition to bleed. 


158 MANUAL OF THE PRACTICE OF MEDICINE. 


Haemoglobinuria and haematuria are common, but there 
may be hemorrhages from any of the free mucous mem¬ 
branes or under the skin. 

Illustrative Cases. —(1) An unknown man fell unconscious 
in the street at 1 p. M. Temperature 97.2 F. Spleen enlarged. 
Plasmodia in blood. Temperature rose to 102.8° F., and the 
coma continued until his death at 7 p. m. 

(2) A sailor just arrived from Cuba. First day. Became 
suddenly unconscious in the street. Temperature 103.2° F., 
pulse 92. Spleen large. Plasmodia found. Ordered qui¬ 
nine, gr. v every two hours hypodermically. Second 
day. Emerged from coma. Temperature normal. Feels 
and acts stupid. Third day. 2 p. m., chill, fever of 106 0 F., 
and acute mania requiring restraint, changing into coma. 
Quinine increased to gr. x every two hours. Fourth day. 
Entirely recovered. Had no more attacks. 

(3) A sailor back two days from Panama. First day. Chill. 
Temperature 105 0 F.; respiration 36; pulse 112. Complete 
coma. Spleen large. Plasmodia found. Ordered quinine, gr. 
x every two hours hypodermically. Second day. Emerged 
from coma by morning, but complained of pain in the stom¬ 
ach; vomiting, and vomiting of blood. Third day. Entirely 
recovered. 

3. Remittent lever. —In this form the temperature does not 
at any time in the twenty-four hours become normal, but 
though there are marked remissions there always is a cer¬ 
tain amount of fever. The onset may be abrupt or may be 
preceded by prodromal headache and malaise for several 
days. In some cases it follows an attack of ordinary inter¬ 
mittent fever. The onset is usually marked by a chill, which 
may be severe. The temperature, once begun, continues 
with remissions. Mild cases run between ioi° and 103° F., 
severe cases between 103° and 106° F. The remissions are 
usually in the early morning, and they are often accom- 


MALARIAL FEVER. 


159 


panied by sweating. With the fever are headache, pros¬ 
tration, constipation, and diminished urine of high specific 
gravity. During the first few days the remissions are well 
marked, ranging from 2° to 3 0 , but as the disease goes on 
the temperature becomes more continuous, although in 
milder cases the remissions may still be decided. As the 
disease subsides the remissions become more and more 
marked, and the temperature may become intermittent. In 
some cases there may be two daily remissions. The dura¬ 
tion is usually from one to three weeks, and the attack 
may terminate in recovery or in death, or the disease may 
merge into intermittent fever. 

Variations in Type. — [a) In mild cases the symptoms are 
not severe; the patient is up and about, and recovers in 
about two weeks. (< b ) In severe cases the temperature has 
a high range; the patient passes into a typhoid condition 
in which he may die in two or three weeks, (c) “ Hemor¬ 
rhagic ” cases are characterized by a tendency to bleed. The 
most common sources of hemorrhage are the kidneys and 
the intestines. Considerable blood in this way may be lost. 
This form is usually seen only at certain times and in certain 
places, (d) In some cases there is developed well-marked 
jaundice, the so-called “ bilious remittent fever.” This fever 
is usually developed during the first week of the disease, and 
is often associated with the hemorrhagic form. The associa¬ 
tion of fever, hemorrhages, and jaundice closely resembles 
yellow fever, and the diagnosis is at times difficult, as both 
diseases are apt to occur at the same time and in the same 
place. Blood-examination should, however, clear the diag¬ 
nosis by finding the plasmodia. 

4. Pernicious Remittent Fever .—This type corresponds 
with pernicious intermittent fever, except that the tempera¬ 
ture at no time in the twenty-four hours comes entirely 
to normal. No further description, therefore, is necessary. 


l 60 MANUAL OF THE PRACTICE OF MEDICINE. 


5. Malarial Cachexia .—This form usually follows pro¬ 
longed attacks of intermittent fever improperly treated. 
Cases developing without such a history are uncommon 
except in intensely malarial districts. The general health 
becomes affected; there is loss of flesh and strength; the 
blood shows marked anaemic changes; the complexion is 
muddy or lemon-colored. The spleen is distinctly en¬ 
larged and firm on palpation. The temperature may be 
normal or subnormal, but there is usually an irregular fever 
of moderate intensity. Digestive disturbances are common. 
There may be functional disturbance of the liver, gastric or 
intestinal indigestion, or irregular action of the large intes¬ 
tine. In other patients neuralgia is a marked symptom. 
Headache is the most common symptom, being frequently 
periodic. The next most frequent symptom is supraor¬ 
bital neuralgia. The degree to which the symptoms are 
developed varies. In rare cases paraplegia or orchitis may 
develop. 

Diagnosis. —The diagnosis of all forms of malaria is 
rendered simple by the finding of the plasmodia in the 
blood and by the subsidence of the disease upon the 
administration of quinine. The chills, the paroxysms of 
fever, and the sweatings of pyaemia, tuberculosis, and 
ulcerative endocarditis might be mistaken for malarial fever. 
Intermittent is to be distinguished from remittent fever by 
the careful use of the thermometer. Remittent fever may 
be mistaken for typhoid or for yellow fever. The diag¬ 
nosis of the pernicious form is often difficult, but the ex¬ 
amination of the blood, the enlargement of the spleen, 
the history of an intense tropical malarial exposure, and 
the results of quinine therapy afford positive diagnostic 
indications. 

Prognosis.— -The prognosis depends upon the severity 
of the infection, upon the proper treatment, and upon pro- 


MALARIAL FEVER. 


161 


longed residence or further exposure in a malarial locality. 
The simple intermittent and remittent fevers do well, 
although if neglected they may run into malarial cachexia. 
The pernicious forms are exceedingly dangerous. A 
patient untreated rarely survives the third paroxysm. If 
energetically cinchonized, the prognosis is fairly good. 
The prognosis of malarial cachexia depends largely upon 
the patient’s ability to change his residence to some locality 
where he will no longer be exposed to the miasm. 

Treatment.— Prophylaxis .—Inhabitants of malarial districts 
should select the situation of their houses, should sleep, if 
possible, upon upper floors, and should avoid night air. It 
is well to take from 6 to 8 grains of quinine after breakfast. 

The arrest of a paroxysm is important only in per¬ 
nicious cases. A full dose of opium (-^ grain of morphine 
hypodermically), grain of pilocarpine hypodermically, 
or a drachm dose of chloroform is often of service. Qui¬ 
nine is useless unless given hypodermically, as its action 
otherwise is too slow. In pernicious cases, however, it 
should be given hypodermically in full doses, the tannate, 
hydrochlorate, or hydrobromate of quinine being given in 
aqueous solution. At least 15 grains should be given every 
two hours in bad cases until the paroxysm yields. 

During the paroxysm the chill and the fever should be 
treated on general principles. 

To prevent recurrences quinine is a specific. It may be 
given in solution or in freshly-prepared capsules or pills. 
Children take it well in chocolate tablets. The dose depends 
upon the severity of the attack and the susceptibility of 
the patient. In mild cases from 10 to 20 grains daily will 
suffice. In severer cases from 20 to 40 grains will be 
required. It may be given in divided doses during the 
twenty-four hours, or in single large doses six to eight hours 
before the expected paroxysm. In severe cases the latter 
11 


162 MANUAL OF THE PRACTICE OF MEDICINE. 


form of administration is preferable. Cinchonism may be 
controlled by phenacetine or sodium bromide. In many 
cases it is best to precede quinine treatment by a mild mer¬ 
curial purgative. The effect of quinine is either to prevent 
paroxysms or to modify their severity or to postpone the 
paroxysm for several hours. A third paroxysm is not to 
be expected. In long-continued cases quinine seems to lose 
its power, and capsules of desiccated Warburg’s tincture 
should be given. Six to eight capsules, each representing 
3 j of the tincture, should be given daily. Good results 
frequently follow the use of arsenic, especially if combined 
with iron and laxatives in small doses, with or without 
small doses of quinine. 

In remittent fever daily doses of from 15 to 20 grains of 
quinine frequently benefit the patient by the third or fourth 
day. In other cases, especially if the remissions be slight, 
quinine does no good, and in these cases it seems best to 
wait until the temperature becomes more markedly remit¬ 
tent, and then quinine regains its curative power. In bad 
cases it is best to continue the use of quinine whether it 
seems to do good or not. 

Treatment of Malarial Cachexia .—The hardest cases to 
treat are those living constantly in some malarial locality. 
The anaemia demands treatment by iron and arsenic, with 
small doses of laxatives if needed. A good combination is 
the following: 

3 ^. Ferri redacti, gr. ij; 

Pulv. ipecac., gr. f ; 

Acid, arseniosi, cr r 1 • 

Ext. colocynth. co., gr. ij.—M. 

Ft. pil. No. j. Sig. Take one three times daily. 

Digestive disorders are to be met with appropriate treat¬ 
ment. Periodical neuralgia may be benefited by quinine, 


ANTHRAX. 163 

arsenic, or Warburg’s tincture. Obstinate cases should be 
sent to some non-malarial locality. 

ANTHRAX. 

Definition and Synonyms.—Anthrax is an infectious 
disease caused by the anthrax bacillus. Synonyms: Malig¬ 
nant pustule ; Malignant oedema ; Splenic fever ; Charbon ; 
Milzbrand ; Woolsorter’s disease. 

Etiology.—Anthrax which is primarily a disease of cattle, 
sheep, and horses, is occasionally communicated to man. It 
is especially frequent in Russia, Siberia, in parts of Europe, 
and in South America. The bacillus of anthrax was the 
first specific micro-organism ever described. It is a rod 
bacillus two to ten times longer than the diameter of a red 
blood-cell, non-mobile, with abundant spore-growth. The 
rods are often jointed together, forming long filaments. 
The bacilli are readily destroyed, but the spores are ex¬ 
ceedingly resistant, and live for a long time in the grass or 
on the surface of pasture-land. Cattle acquire the disease 
by eating the infected grass or by inhaling the spores. 

In man the disease may be acquired by inoculation, by 
inhalation, or by the alimentary canal. Inoculation results 
from handling infected hides, wool, hair, or instruments, or 
by bites of flies or of mosquitoes. The disease may be ac¬ 
quired by inhalations from infected skins or wool, or the 
alimentary canal may be infected from diseased meat. 

Symptoms.—The disease occurs in an external and an 
internal form. 

I. External Form. — (a) Malignant pustule is the most 
common form, and it occurs from inoculation of an ex¬ 
posed surface, usually the face. Symptoms begin from a 
few hours to four days after inoculation, with itching, 
pricking, or burning like the sting of an insect. A papule 
is formed, developing into a vesicle which ruptures, dis- 


164 manual of the practice of medicine. 


charges bloody serum, and leaves a spot of brown dry 
gangrene surrounded by a zone of red swollen skin which 
may be covered by vesicles and which resembles a carbun¬ 
cle. There is brawny oedema of the subcutaneous tissues 
that may involve the whole of an arm or the side of the 
neck within thirty-six hours. There are usually lymphan¬ 
gitis and phlebitis starting from the infected areas. 

Constitutional symptoms occur if the infection becomes 
general. These symptoms are usually delirium or a tran¬ 
quil mind, fever, sweating, vomiting, collapse, and death, 
from heart failure or in the typhoid condition, in from five 
to eight days. If general infection does not occur, the 
constitutional symptoms are those which ordinarily accom¬ 
pany a local inflammation. 

The prognosis is exceedingly grave, although in a large 
number of patients who recover the slough separates and 
the wound heals. The mortality is greatly reduced if rad¬ 
ical treatment be resorted to at the onset. 

(b) Malignant Cddema .—This form occurs in regions 
where the connective tissue is loose, as the eyelids, neck, 
and forearm. The skin may not be discolored, but there is a 
flat infiltration with ill-defined borders and a rapidly-spreading 
oedema which may be of sufficient intensity to cause gan¬ 
grene. Constitutional symptoms occur early, and the disease 
is almost invariably fatal, although recovery is possible. 

2 . Internal Form. — (a) Intestinal Form (Mycosis Intesti- 
nalis).—This form of anthrax is caused by eating infected 
meat, and it may affect a number of people at the same 
time. The attack begins as an acute infection with a chill, 
fever, pain in the head and back, with severe gastro-intestinal 
symptoms, vomiting, and diarrhoea. There is a tendency 
to hemorrhages, and metastatic malignant pustules may 
occur on the skin. There may be delirium or convulsions. 
Dyspnoea and cyanosis are common, and death from heart 


ANTHRAX 


Plate 14 



Bacillus anthracis : cover-glass preparation from spleen of white mouse {American Text 

Book 0/ Surgery). 






HYDROPHOBIA . 165 

failure occurs in a few days. These cases are invariably 
fatal. 

(b) Woolsorters ’ Disease .—These cases result from sorting 
and picking infected hair and wool. There is a chill, fol¬ 
lowed by fever, pains in the head and chest, dyspnoea, and 
cough. Vomiting and diarrhoea are common. There may 
be a clear and tranquil mind, although delirium and uncon¬ 
sciousness are frequent. There is increasing heart weak¬ 
ness, and death results, in collapse and extreme prostration, 
in from one to seven days. 

Treatment. —Preventive treatment should be directed to 
cattle and sheep. Diseased animals should be killed and 
buried deeply or cremated; suspected animals should be 
isolated. Inoculations with attenuated virus are being em¬ 
ployed with considerable success in securing immunity. 

In man the only form amenable to treatment is the exter¬ 
nal pustule. The mass should be excised thoroughly or be 
penetrated by deep crucial incisions into which powdered 
bichloride of mercury is to be sprinkled. Subcutaneous 
injections of a solution of carbolic acid or of a bichloride-of- 
mercury solution may be made about the pustule and be 
repeated two or three times a day. 

HYDROPHOBIA. 

Definition and Synonym. —Hydrophobia is an acute 
specific disease of animals, and is communicated to man by 
inoculation. Synonym: Rabies. 

Etiology. —All animals are susceptible, but the disease is 
most common in the dog, wolf, cat, skunk, and fox. There 
is undoubtedly a microbe of the disease, but it has not yet 
been demonstrated. The poison is found in the neivous 
system and the secretions, especially in the saliva. The 
affection is acquired in man by bites of rabid animals 01 by 
the inoculation of abraded surfaces with the saliva. It 


166 MANUAL OF THE TEACTICE OF MEDICINE. 


occurs more readily in children than in adults, and infection 
is most certain in wounds of the face and head and in cases 
of severe and lacerated bites affording extensive surfaces for 
absorption. Infection is more severe in the bites of wolves 
than in those of cats or dogs. Of persons bitten by rabid 
dogs, from 15 to 50 per cent., according to various author¬ 
ities, become affected by the disease. The infecting saliva 
may be absorbed by the clothing if the bite is inflicted 
upon a clothed part. In this case infection may not 
occur. 

The incubation period varies from six weeks to two months 
in ordinary cases. It may be as short as two weeks, or be 
protracted for several months, but never longer than eight 
months. Cases with incubation of from one to two years 
have -been reported, but they are not well authenticated. 

Pathology.—Little or no lesion may be found at autopsy. 
Congestion of the blood-vessels, perivascular exudation of 
leucocytes, and minute hemorrhages may be found in the 
brain and spinal cord. These are the most characteristic 
lesions, and are particularly well marked in the medulla. 
There may be congestion of the pharynx and of the mu¬ 
cous membrane of the respiratory and gastro-intestinal 
tracts. 

Symptoms.—There are three stages of the disease. 

1. Premonitory Stage .—The onset is usually preceded by 
irritation, pain, or numbness in the cicatrix, which may be¬ 
come congested and tender. The patient passes into a con¬ 
dition of mental depression and melancholia, becomes irri¬ 
table and sleepless, and is in a condition of extreme anxiety. 
The special senses are keenly alert. This stage lasts about 
a day. 

2. Spasmodic Stage .—The first characteristic symptom 
is inability to swallow, from spasm of the muscles of deglu¬ 
tition whenever the act is attempted. The spasm spreads 


HYDROPHOBIA. 


167 


to the laryngeal muscles of respiration, causing dysp¬ 
noea and the utterance of odd barking sounds. Breathing 
in consequence becomes painful and embarrassed. 1 he 
spasms, excited at first by attempts at swallowing, finally 
are produced by any afferent stimulant, such as draughts 
of air, sounds, or even mental suggestion, and extend to 
involve the muscles of the body generally. During these 
convulsions the patient snaps with his mouth and ejects 
foaming saliva in every direction. Mania often accompanies 
the spasms, while in the intervals the mind is usually clear, 
though distressed by fearful dread of impending death. 
Profuse salivation is common. The temperature is usually 
elevated, although it may be subnormal. The pulse becomes 
increasingly rapid, feeble, and intermittent. Prostration be¬ 
comes more marked after each paroxysm. There may be 
death from asphyxia in any of the paroxysms. This stage 
usually lasts for from one to three days. 

3. The paralytic stage lasts for from six to eighteen hours. 
The patient becomes quiet, the spasms cease, and the patient 
may swallow with ease. Unconsciousness is gradually de¬ 
veloped, and death from cardiac failure occurs. 

Prognosis. —Much can be done by preventive inocula¬ 
tions in the stage of incubation. When the disease, how¬ 
ever, has once begun, it is invariably fatal. 

Treatment. —Immediately after a person has been bitten 
a ligature should be applied on the proximal side, and the 
wound be sucked energetically, provided there be no cari¬ 
ous teeth or abrasions of the mouth or lips of the operator. 
The best results have followed an immediate excision of the 
wound succeeded by thorough disinfection. Cauterization 
is not so certain as excision as a method of prevention. 

Preventive Inoculations .—Pasteur found that the contin¬ 
uous inoculation of the virus from rabbit to rabbit increased 
its strength to a maximum virulence, while gradual desic- 


168 MANUAL OF THE PRACTICE OF MEDICINE . 


cation of the medulla containing the virus diminished its 
virulence so that after two weeks’ desiccation the virus 
became innocuous. It is possible, then, to obtain the virus 
in any grade of virulence. 

Inoculations were made in dogs, beginning with injections 
of an emulsion of the non-virulent medulla, followed by 
those of increasing strength until injections of medullas 
of the greatest virulence could be made with impunity. 
Animals so treated became immune to hydrophobic infec¬ 
tion. 

The same series of injections are now made in the case 
of those who have been bitten by rabid animals (although 
in men the final injections used are not of the most virulent 
quality), with the result that the occurrence of hydrophobia 
in nearly all cases is prevented. The mortality of those 
bitten by rabid animals and treated in this manner has been 
reduced to 0.60 per cent. 

There is another method of antirabic vaccination proposed 
—the gradual inoculation of an innocent virus obtained by 
the action of gastric juice upon the cords of infected rabbits. 
This method has even cured the developed disease in rab¬ 
bits, but it has not yet been tried in man. 

Treatment of the Disease .—When hydrophobia develops 
the spasms can be relieved only by morphine hypodermics 
and by inhalations of chloroform. The patient in this way 
is made more comfortable until he dies. 

Pseudo-rabies is an hysterical condition occurring in 
persons who have been bitten by dogs supposedly rabid, 
and it may closely simulate true hydrophobia. The symp¬ 
toms develop frequently too long after the bite to be real 
rabies; the temperature is not elevated ; the disease is of 
longer duration and is amenable to antihysterical treatment. 
The diagnosis is corroborated by the knowledge of the fact 
that the dog was not rabid. 


TETANUS. 


169 


TETANUS. 


Definition and Synonyms.—Tetanus is an infectious 
disease due to a specific bacillus. It is characterized by 
painful tonic spasms of the volun¬ 
tary muscles with exacerbations. 

Synonyms: Trismus; Lock-jaw. 

Etiology.—The bacillus appears 


t 




/ 


\ 




X 


Fig. 3.—Bacillus tetani (cover- 
glass preparation from culture by 
Kitasato). 


as a delicate rod swelling at one 
extremitv to contain a shining 
spore, assuming thus the appear¬ 
ance of a drum-stick or a pin. 

Pure cultures are obtained with 
difficulty. Injections of the germs, or even of the sterilized 
or filtered cultures, cause tetanus convulsions. Brieger has 
lately isolated from tetanus cultures their distinct toxines, 
tetanine, tetanotoxine, and spasmotoxine, which act on the 
nervous centres as does strychnine, causing convulsions 
and spasms. 

The bacilli are found in various kinds of surface soil and 
street dust. In warm climates the soil acts as an excellent 
culture medium, hence in these localities the disease is 
more common than in colder climates. The bacilli may 
thrive in some particular soil so that the disease becomes 
endemic in that place, as in the east end of Long Island. 
It may assume epidemic proportions in institutions, in 
hospitals, and during wars. The colored race is especially 
susceptible. 

To acquire the disease the germ must enter through an 
abraded or a broken cutaneous or mucous surface. It may 
follow wounds, especially of the hands and feet, or it may 
infect the umbilicus in newly-born children (tetanus neona¬ 
torum). It frequently follows frost-gangrene. In some 
cases the point of entrance is so slight as readily to be 


I70 MANUAL OF THE PRACTICE OF MEDICINE. 

overlooked. These cases are designated “ idiopathic 
tetanus.” 

The bacilli are found in the wound-secretions, in the 
nerves leading from the point of infection, and in the spinal 
cord of the patient. 

Pathology. —There are no distinct morbid changes. 
There may be seen congestion, perivascular exudation, and 
granular degeneration of the nerve-cells in the brain and 
spinal cord. There may be redness and swelling of the 
nerve-trunks. In tetanus of the new-born there may be 
inflammation of the umbilicus. 

Symptoms. —The period of incubation is about two 
weeks, although from one to twenty-one days constitute its 
limits. The symptoms begin insidiously with soreness 
about the neck and pain and stiffness in the muscles. Then 
develops the characteristic spasm of the muscles of masti¬ 
cation. This trismus, or lock-jaw, is almost pathogno¬ 
monic, provided local causes for spasm can be excluded. 
The spasm then spreads to the muscles of the back of the 
neck, of the face, and of the trunk. The head is drawn 
backward and held rigidly; the face has a mask-like 
appearance due to immobility; the corners of the mouth 
are drawn back, giving the “ sardonic grin.” The forehead 
is wrinkled, the patient having a peculiarly aged appear¬ 
ance. The spasm of the spinal muscles may arch the body 
backward so that the patient is supported only by the head 
and the heels (opisthotonos), and less frequently the body 
may be flexed forward (emprosthotonos) or curved to either 
side (pleurosthotonos). In severe cases the body is entirely 
straight and stiffened from general muscular spasm (or- 
thotonos). The legs may be in a condition of spasm, but 
the arms more frequently can be moved freely. 

The affected muscles are in a condition of tonic rigidity 
interrupted now and then with violent clonic spasms. 


TETANUS. 


171 


These spasms may be so severe as to tear the rectus ab- 
dominalis. The muscles are exquisitely painful and tender, 
especially during a paroxysm. 

The paroxysms are reflex, and are produced by any 
slight stimulus, such as a noise, a jar, or a draught of air. 
In some cases they may appear to be spontaneous. 

If the intercostal muscles are affected, there is embar¬ 
rassed respiration with dyspnoea and cyanosis. These 
symptoms are so aggravated, should the diaphragm be 
involved, that the patient rarely survives the second or 
third tetanic spasm. 

In rare cases the muscles of deglutition are involved. These 
cases are spoken of as “ hydrophobic tetanus ” or the “ head- 
tetanus ” of Rose, and follow injury of the face. Besides the 
trismus and the difficult deglutition there is apt to be paral¬ 
ysis of the facial nerve on the side of the injury. 

The temperature is always elevated in acute cases, usually 
running to 104° F. or even higher. There maybe a marked 
rise of temperature after death. In the milder and more 
chronic cases there may be but slight fever or the tempera¬ 
ture may be normal. The pulse becomes rapid and feeble 
toward the close of the disease. The mind is clear through- 

o 

out. There is usually profuse perspiration. 

The duration varies. The acute forms may be fatal in 
from one to seven days. If the attack be mild, there may 
be but little spasm of the muscles of the trunk, and consti¬ 
tutional disturbances are not marked. In these cases tris¬ 
mus is the principal symptom. These mild cases run a 
course for a number of weeks. 

Diagnosis. —Tetanus should not be confounded with the 
following conditions: 

1. Strychnine-poisoning .—Here the maximum symptoms 
are developed suddenly, the muscles not being involved in 
gradual order as in tetanus. Trismus is absent and the 


172 MANUAL OF THE PRACTICE OF MEDICINE. 

arms are involved. Between the spasms the muscles are 
relaxed, and not rigid as in tetanus. The course is shorter 
than that of tetanus. 

2. Hydrophobia .—Here there are the history of the case, 
involvement chiefly of the muscles of deglutition, and 
absence of trismus. 

3. Hysteria .—The convulsions are not limited to any 
special group of muscles; there is no trismus; between the 
spasms there is muscular relaxation; there is no change in 
temperature or pulse; other hysterical symptoms are pres¬ 
ent ; the spasms are irregular and more spontaneous than 
reflex. 

Prognosis.—The disease is fatal in 80 per cent, of trau¬ 
matic cases and in 50 per cent, of idiopathic cases. It is 
almost always fatal in infants. Most of the cases of hydro- 
phobic tetanus recover. When the incubation period is less 
than ten days, the mortality is 96.6 per cent. 

Treatment.— The patient should be kept in a darkened 
room from which all sounds and other causes of irritation 
are to be excluded absolutely. No talking or unnecessary 
movements are to be permitted. If the trismus prevents 
the patient from taking even fluid food, he may be fed 
through a tube or by the rectum. To relieve the spasms 
morphine hypodermically is the most satisfactory drug. 
In milder cases chloral combined with sodium bromide may 
be employed. In very severe cases inhalations of chlorotorm 
may be necessary. In mild cases the use of hot baths may 
be of service. Woorara, which has been employed fre¬ 
quently, is not recommended, because of its depressing 
effect on the heart. In all cases the infected wound must 
be disinfected to prevent further absorption. Scars may be 
excised and foreign bodies be removed. Nerve-stretching 
and nerve-section have proved disappointing. 

The hope of successful treatment lies in the use of anti- 


LEPROSY. 


173 


toxines derived from the blood-serum of animals rendered 
immune. Immunity is procured by the injection of germ 
cultures treated with trichloride of iodine. The injection 
of the blood-serum of such immune animals into persons 
suffering from tetanus has frequently been followed by a 
prompt recovery, while in almost all cases the severity of 
the disease has been modified greatly. 

LEPROSY. 

Definition.—Leprosy is a chronic infectious disease due 
to the bacillus leprae and characterized by tubercular 
nodules of the skin and the mucous membranes and by 
changes in the nerves. 

Etiology.—At present the principal centres of leprosy 
are India, China, and the Sandwich Islands. Other import¬ 
ant foci are Norway, the Baltic provinces of Russia, 
Mexico, certain parts of Central and South America, and 
the West India Islands. In North America it occurs in 
certain of the Gulf cities, especially New Orleans, in the 
province of New Brunswick, and along the Pacific coast, 
where it occurs chiefly among the Chinese. Isolated cases 
occur from time to time in all large cities. 

The disease may be called “ contagious,” but only in the 
sense that direct inoculations are necessary, as is the case 
with syphilis. It may be congenital or hereditary, and it 
may be acquired through sexual congress. The majority 
of cases occur from the fifteenth to the thirtieth year. The 
specific cause is the bacillus leprae, discovered in 1874 by 
Hansen. This bacillus, which closely resembles the 
tubercle bacillus but may be distinguished from it, can be 
cultivated; but while inoculations of the leprous nodules 
can reproduce the disease, inoculations of the pure bacillus 
cultures have produced only negative results. 

Pathology.—The leprous nodules consist of aggregated 


174 MANUAL OF THE PRACTICE OF MEDICINE. 

lymphoid, epithelioid, and giant cells in and among which 
are found numerous bacilli. The nodules may in rare cases 
become organized and encapsulated, but they have a tend¬ 
ency to break down, discharge puriform matter, and result 
in ulcers which may heal in one direction while spreading 
in another. In the nerves the bacilli cause neuritis. In the 
last stages of the disease leprous nodules may be found in 
internal organs, especially the spleen and the liver. 

Symptoms.—Two forms are described, which may 
occur separately or be combined in the same patient: 

1. Tubercular Leprosy .—There appear on the skin hyper- 
aesthetic patches of sharply-defined erythema that become 
gradually darker from pigmentation. These patches which 
precede the nodules are designated as “ macular leprosy.” 
In some cases they subsequently become anaesthetic and 
lose their pigment, white spots being left, the “ white 
leprosy.” Nodules then develop in the skin of any part of 
the body excepting the scalp, and in the mucous mem¬ 
branes, especially of the mouth, throat, larynx, and con¬ 
junctiva. The nodules vary in size from a pea to a walnut, 
and coalesce. This is especially marked in the face, the 
term leontiasis being applied to the thickened and distorted 
features so caused. 

The skin over the nodules is tense and glistening and 
may become red and painful. The hairs of the affected 
areas drop out, the loss of the eyebrows being a suggestive 
symptom. From the softening and breaking down of the 
nodules there are caused extensive ulcerations frequently 
covered with crusts. The ulceration may extend to the 
bones, causing falling of the bridge of the nose or loss of 
the fingers or toes, or there may be total destruction of the 
eyeball. 

2. Ancesthctic leprosy occurs when the nerve-trunks are 
involved. There are at first areas of hyperaesthesia and 


LEPROSY. 


I 


75 



Tubercular leprosy in a 


patient twenty years old (Goldschmidt). 






































176 MANUAL OF THE PRACTICE OF MEDICINE. 

neuralgic pains, followed by anaesthesia over moie 01 less 
extensive surfaces. The anaesthetic spots following the 
macules have already been alluded to. If the larger nerve- 
trunks are involved, they may be felt as nodulai coids. 
Suppression of sweating occurs in the affected areas. 

There are trophic changes. Bullae may form at any time, 
and after discharging their contents may either heal or be 
converted to extensive ulcers. There may be perforating 
ulcer of the foot or loss of the phalanges of the fingers or 
the toes. Paralyses, contractures, and atrophy of muscles 
are commonly observed. 

The prognosis is bad, but not absolutely hopeless. The 
average duration of the tubercular cases is from eight to 
ten years; of the anaesthetic cases, fifteen to twenty years. 

Treatment. —Patients should live in isolated communities 
and under the best hygiene. Their general health and nutri¬ 
tion must be superintended carefully. 

There is no specific medication. Iodide of potassium in 
full doses (falling short, however, of iodism) and arsenic 
have been recommended. Of late gurjun oil in 10-minim 
doses and chaulmoogra oil in 2-dram doses have been 
favorably regarded. The former may be given by the 
mouth or by inunction. 

GLANDERS. 

Definition and Synonym. —Glanders is an infectious 
disease of the horse, ass, and mule, communicable to man. 
Synonym : Farcy. 

Etiology. —The disease is due to a specific bacillus, the 
bacillus mallei, which is short and non-motile, closely 
resembling the tubercle bacillus. The bacillus can be 
cultivated, and causes the disease by inoculation. The 
disease is acquired in man by contact of the nasal dis¬ 
charges of the horse with an abraded mucous or cutaneous 


GLANDERS. 


177 


surface. In rare cases it results from inhalation of the 
desiccated discharges. The disease is also transmissible 
from man to man. It occurs chiefly in those who have to 
do with horses. 

Lesion.—The lesion consists in the formation of little 
tumors composed of epithelioid and lymphoid cells among 
and in which are found the bacilli. The lesion is really a 
variety of infective granuloma. The nodules tend to 
break down rapidly, causing ulcers when they occur in the 
mucous membranes (glanders), and abscesses when they 
occur in the skin, the muscles, or the internal viscera. The 
adjacent skin, lymphatics, and mucous membrane are 
inflamed. 

Symptoms.—The symptoms begin in from three to five 
days after inoculation, but may be delayed for three weeks. 
An acute and a chronic form may be recognized in man. 

1. Acute Glanders .—There are at the onset malaise, head¬ 
ache, fever, and pain in the limbs, resembling the onset of 
typhoid fever, for which it is often mistaken. In peracute 
cases the onset is that of a more severe general infection. 
The local symptoms may be of the “ farcy ” or of the 
“ glanders ” type. 

Farcy Type .—The infected part becomes red, swollen, 
and painful, the inflammation becoming widely diffused; 
there are developed nodules which become abscesses. These 
latter may rupture, leaving irregular deep ulcers with a 
grayish infiltrated floor which may become necrotic. These 
suppurating nodules are frequently mistaken for small-pox. 
The lymphatics are early affected, and along their course 
are subcutaneous nodules, the so-called “ farcv-buds.” 
There may be swelling and suppuration of the joints. 
Abscesses may form in the muscles. 

Glanders Type .—There is a purulent, blood-stained, fetid 
discharge from the nose, with a spreading inflammation of 
12 


178 MANUAL OF THE PRACTICE OF MEDICINE. 


the skin over the nose and the face somewhat resembling 
erysipelas. Examination shows the nasal cavities to be 
deeply ulcerated. The septum may be necrosed. There 
may be similar ulcerations in the mouth, pharynx, larynx, 
and bronchi. Usually in man both sets of local symptoms 
are found. 

Constitutional symptoms are those of an intense infection. 
The temperature rises and may assume the pyaemic type, 
with remissions and irregular rises accompanied by chills 
and sweating. The pulse becomes rapid and steady, the 
tongue brown and dry. Vomiting and diarrhoea are almost 
constant. Pneumonia is apt to develop. There are restless¬ 
ness and delirium at first, passing into stupor and coma, 
while death results in the typhoid condition in from eight to 
fourteen days. Peracute cases may live but a few days. In 
mild cases the local symptoms are less severe and the gen¬ 
eral infection is slight and limited, so that the course is mild 
and recovery is possible. The cases in which the nose is 
extensively involved—glanders type—are invariably severe 
and fatal. 

2. Chronic Glanders .—The disease is insidious, resemblinsr 

7 o 

ozaena or nasal syphilis. There is a fetid, purulent discharge 
from the nose, with intractable ulcerations. There are also 
subcutaneous nodules, abscesses, and ulcers without much 
inflammatory reaction or involvement of the lymphatics. 
These cases may last for months or even years, and usually 
recover, although at any time the acute form may be de¬ 
veloped with a fatal issue. 

Treatment.—In the early stages the wound should be 
excised or cauterized and treated antiseptically. For the 
acute cases little can be done. The nasal passages should 
be kept cleansed by injections of weak antiseptic solutions. 
Abscesses and farcy-buds should be opened as early as 
possible. 


A C TINOM YC OS IS. 


179 


ACTINOMYCOSIS. 

Definition. —Actinomycosis is a form of chronic inflam¬ 
mation caused by the actinomyces, or ray fungus. 

Etiology. —Actinomycosis is a disease primarily of cattle, 
pigs, or horses, acquired in man by inoculations through 
abrasions of the skin, of the mucous membrane of the mouth, 
or through carious teeth. The fungus may be taken into 
the alimentary canal in contaminated water, in the flesh of 
the pig, or in infected cereals. 

The ray fungus, or actinomyces, consists of threads with 
bulbous extremities radiating from a common centre, form¬ 
ing a globular rosette. In man the fungi appear as little 



Fig. 4. —Actinomyces (Von Jaksch). 


round masses the size of a millet-seed, usually of a sulphur- 
yellow color. They are found in the tumors and in the 
purulent discharges, and can be cultivated and inoculated. 

Pathology.—The lesion consists in the transformation 
of mature connective tissue into embryonal or granulation- 
tissue composed of round and epithelioid cells sometimes 
containing giant-cells. The appearances are identical with 
those of sarcoma or tubercle, but in the tumors the cha¬ 
racteristic ray fungus is found. The tumors show a tend- 


l 80 MANUAL OF THE PRACTICE OF MEDICINE. 


ency to break down and suppurate, forming abscesses and 
sinuous fistulae. There is a chronic inflammation of 
the surrounding structures, but the lymphatics are not 
involved, and the course of the disease resembles that 
of a malignant tumor more than that of an acute 
infection. 

Symptoms.— i. Alimentary Actinomycosis. —The upper or 
lower jaw is frequently involved. There is considerable 
swelling and enlargement of the bone resembling osteo¬ 
sarcoma ; sinuses are common, tending to invade the ad¬ 
jacent soft structures of the neck and the face. The tongue, 
the intestines, or the liver may be involved primarily or by 
metastasis. 

2. Cutaneous Actinomycosis. —There may be slowly-grow¬ 
ing tumors which may suppurate and leave intractable ulcers 
and fistulous tracts. 

3. Cerebral Actinomycosis. —This form is rare. The symp¬ 
toms are those of multiple tumors or abscesses. 

4. Pulmonary Actinomycosis. —Three clinical forms are 
described by Hodenpyl: (a) There may be the lesions of 
chronic bronchitis with the actinomyces in the sputum, (b) 
Small nodules may be scattered in the lungs, resembling 
miliary tuberculosis, (c) The lesions may be more exten¬ 
sive—broncho-pneumonia, interstitial pneumonia, large ab¬ 
scesses. In some cases there may be abscesses of the chest- 
wall that may be mistaken for empyema. 

The prognosis is good if the disease be recognized early 
and if the infected locality be amenable to surgical treat¬ 
ment. Spontaneous recovery does not occur. The prog¬ 
nosis of internal actinomycosis is bad. 

Treatment is entirely surgical, consisting in the excision 
or cauterization of the diseased masses and in opening and 
disinfecting abscesses and sinuses. Injections of weak anti¬ 
septics into diseased internal tissues may be made. 


WEIIJS DISEASE. 


181 


MILK SICKNESS. 

This disease occurs west of the Alleghany Mountains and 
is associated with the “ trembles ” in cattle. It is communi¬ 
cated to man by infected meat or milk, also by butter and 
cheese. The animals subject to the disease are cattle, lambs, 
and colts. The disease is most frequent in new settlements, 
and with the advance in civilization is rapidly becoming 
extinct. 

The pathology is unknown. 

The symptoms in cattle are refusal of all food, in¬ 
jected eyes, marked tremors or “ trembles,” and death in 
convulsions. 

The symptoms in man begin with abdominal pain, nau¬ 
sea, and vomiting. There is intense thirst with fever. The 
breath becomes peculiarly offensive. The tongue is swollen 
and tremulous. Cerebral symptoms develop—restlessness, 
delirium, and coma; the patient passes into the typhoid 
state and dies. Acute cases last for two or three days; 
subacute cases continue for two or three weeks. 

The treatment is entirely symptomatic. 

WEIL’S DISEASE. 

This disease was first described in 1886 by Weil, and 
bears his name. The exact nature of the disease is un¬ 
known. It is most common in the summer months, when 
small epidemics may appear. It attacks males more fre¬ 
quently than females, is most common between the ages of 
twenty-five and forty, and butchers seem especially liable 
to it. 

Symptoms. —The onset is acute, being marked by head¬ 
ache, by pain in the back and muscles, and by fever which 
is usually of a pronounced remittent type. Jaundice appears 
early and is of the obstructive form, with clay-covered stools. 


182 MANUAL OF THE PRACTICE OF MEDICINE. 


The liver and spleen are swollen, and the liver is tender on 
palpation. Albuminuria is commonly observed. Gastro¬ 
intestinal symptoms are but rarely observed. Cerebral 
symptoms may appear in severe cases. The duration of the 
disease is from ten to fourteen days. 


II. DISEASES OF THE CIRCULATORY 

SYSTEM. 


I. DISEASES OF THE PERICARDIUM. 

The diseases of the pericardium may be described ana¬ 
tomically and clinically under the following divisions : i. 
Acute plastic or dry pericarditis ; 2. Pericarditis with effu¬ 
sion ; 3. Purulent pericarditis, or empyema of the pericar¬ 
dium ; 4. Chronic adhesive pericarditis; 5. Tubercular peri¬ 
carditis ; 6. Cancerous pericarditis. 

Dry pericarditis and pericarditis with effusion may be 
considered together under the general heading of 

PERICARDITIS. 

Etiology.—Pericarditis is due to infective processes or 
to the extension of inflammation from contiguous organs. 

Primary or idiopathic cases are rare except as the result 
of traumatism either external or from within, as by the 
passage of a foreign body through the oesophagus to the 
pericardium. 

Secondary inflammation is common, from the following 
causes: 

( a ) Pericarditis from extension may complicate various 
diseases of the lung or the pleura, such as pneumonia, 
pleurisy, tubercular disease, or cancer. In double pleurisy 
the pericardium is usually involved. The disease may 
result from the extension of inflammation of the abdominal 
organs, such as peritonitis or abscess of the liver ; it may 
also result from inflammation of the heart-wall, as in 
myocarditis. 


183 



184 MANUAL OF THE PRACTICE OF MEDICINE. 


(/>) Pericarditis is one of the most important complica¬ 
tions of rheumatism, occurring in from 14 to 37 per cent, 
of all cases of the latter disease. The disease may occur 
with either mild or severe forms, may precede the articular 
affections, and often occurs in the abarticular forms of 
rheumatism in children. 

(r) Pericarditis may accompany any of the eruptive 
fevers, especially scarlatina. 

( d ) The disease may complicate any of the septic 
diseases, as pyaemia, puerperal fever, malignant endocar¬ 
ditis, septic thrombi, gonorrhoea, bone necrosis, or in¬ 
fluenza. It is not infrequent in pneumonia. 

(0) Certain dyscrasias render the pericardium susceptible 
to inflammation. Gouty, scorbutic, and diabetic patients 
are liable to pericarditis, while with Bright’s disease peri¬ 
carditis is by no means rare, especially in patients over fifty 
years of age. 

Pericarditis occurs at all ages, but is more common in 
young adults. It may be a disease of intra-uterine life, or 
it may occur in the newly-born from septic infection 
through the navel. In childhood pericarditis is more 
commonly due to rheumatism or scarlet fever, while in 
advanced life it is oftenest associated with the atrophic form 
of Bright’s disease. 

The lesion of pericarditis resembles that of the kindred 
inflammations of the pleura in which the inflammation may 
be plastic with but a small amount of effusion, or may pass 
into the stage in which effusion is abundant and alters the 
clinical course and the physical signs of the disease. The 
inflammatory process, however, is the same, differing only in 
the amount of serum exuded. 

The lesion may be localized or general at the start. The 
base and the anterior surface of the heart are oftenest 
affected. The pericardium becomes dry, congested, lustre- 


PERICARDITIS. 


185 


less, and covered with an exudate of fibrin in the meshes 
of which a certain amount of fluid effusion is entangled. 
The fibrin may be thin and dry like a membrane, under 
which the pericardium appears congested, or it may be in 
long shreds, giving a hairy appearance to the heart—the 
cor villosum; or, if the fibrin is abundant, the pericardium 
may have a ridge-like appearance resembling buttered sur¬ 
faces of bread drawn apart—the “ bread-and-butter pericar¬ 
dium.” This is the lesion of plastic pericarditis. Pericar¬ 
ditis with effusion does not stop here, but an exudate of 
serum containing desquamated and proliferated endothelial 
cells, scanty pus-corpuscles, and flocculi of fibrin is poured 
out to an amount varying from 200 cubic centimeters to 2 
liters. The serum may be admixed with blood in old and 
cachectic patients. This effusion fills the pericardial sac, 
displaces the heart upward and to the left, and may be 
abundant enough to exert pressure on the heart, especially 
the auricles and the venae cavae, the left bronchus, the 
oesophagus, and the lung, or to exert traction on the recur¬ 
rent laryngeal nerve. 

In mild cases the myocardium is turbid and pale to the 
depth of from 2 to 3 millimeters, but in more severe cases 
the myocarditis is more extensive and may endanger the life 
of the patient. Pericarditis is often associated with endo¬ 
carditis, as both diseases are apt to arise from the same 
causes. In rare cases inflammation may spread from the 
one to the other membrane. 

Pericarditis may terminate in the following ways: (1) By 
resolution and absorption of both fibrinous and serous exu¬ 
date. (2) By organization of the fibrin into connective-tis¬ 
sue adhesions. From such an adherent pericardium may 
result hypertrophy and dilatation of the heart, often to an 
extreme degree, chronic interstitial myocarditis, and fatty 
degeneration of the heart. (3) The inflammation may be- 


1 86 MANUAL OF THE PRACTICE OF MEDICINE . 


come chronic. The pericardium becomes thickened by con¬ 
nective-tissue growth and may be infiltrated with salts of 
lime, and the fluid may not be absorbed. This condition is 
especially seen, however, in tubercular cases. 

The symptoms may be divided into four groups: 

1. Inflammatory Symptoms .—An initial chill is rare. 
Fever is not usually high; it may be irregular or absent. 
Hyperpyrexia has been observed in rheumatic cases. Pain, 
which is noted in about three-quarters of all the cases, may 
be distressing and intense, resembling angina, or the patient 
may complain only of a feeling of uneasiness, may be, or 
oppression. The pain may be referred to the precordia or 
to the lower part of the sternum. The pain usually dimin¬ 
ishes as fluid accumulates, but in some cases it becomes 
thereby increased. It may be increased when the patient 
inclines forward or when pressure is exerted upward from 
the epigastrium. There may be tenderness on pressure 
over the precordia. These inflammatory symptoms may be 
slight, the onset of the disease being insidious. There may 
be only a gradual failing in health, slight dyspnoea, and in¬ 
creasing pallor. 

2. Deranged action of the heart is seen in both forms of 
pericarditis, and depends upon the associated myocarditis. 
If there be no myocarditis, the pulse may be rapid and irreg¬ 
ular or strong and tumultuous. In dry pericarditis of a 
small area the pulse may be but slightly altered. If myo¬ 
carditis be extensive, the power of the heart is thereby 
weakened and symptoms of heart failure ensue. The pulse 
becomes rapid, feeble, and irregular; the patient feels faint 
and complains of dyspnoea. In bad cases there may even 
be venous congestions, especially if the venae cavae be pressed 
upon by the distended pericardial sac. The presence of 
venous congestions is almost a proof of the presence of 
myocarditis or complicating endocarditis. 


PERICARDITIS. 


18; 

3. Pressure-symptoms occur with abundant effusion. The 
heart’s action becomes irregular and weak; the veins of the 
neck and the arm may become congested and enlarged. 
Dyspnoea may be aggravated by pressure on the left bron¬ 
chus. Pressure or traction on the recurrent laryngeal nerve 
as it winds around the aorta will produce hoarseness or 
aphonia, laryngeal cough, and dyspnoea which may be spas¬ 
modic and distressing. With large pericardial effusions 
may be observed the pulsus paradoxus, in which the pulse- 
wave is weak or even imperceptible during inspiration. 

4. Symptoms of the primary disease often coexist with 
those of the pericarditis, and may obscure the diagnosis. 
To be on the safe side, the temperature and the pulse should 
be recorded in every disease that may cause pericarditis, 
especially rheumatism and scarlet fever, even into convales¬ 
cence, and physical examinations of the heart should be 
made regularly. There should be special inquiry as to 
pain and dyspnoea. Pericarditis should be suspected in 
every case of Bright’s disease seriously sick with obscure 
symptoms. 

Physical Signs. —Palpation may reveal a friction fremitus 
best marked over the right ventricle. The characteristic 
sign is the friction sound. It is of a rubbing, grating, or 
sticky quality, and may in some cases resemble the creak¬ 
ing of new leather. It may occur during the systole, dur¬ 
ing the diastole, or during both, the last being the most 
common. In rare instances it has a triple rhythm. It is 
not exactly synchronous with the heart sounds, the double 
or to-and-fro movement usually outlasting the first and 
second sounds. The friction sound appears superficial close 
to the ear and is intensified by pressure with the stetho¬ 
scope or by inclining the patient forward. It is heard 
best over the exposed portions of the heart—that is, in the 
fourth and fifth spaces near the sternum. It may, however, 



1 88 MANUAL OF THE PRACTICE OF MEDICINE. 


be heard at the extreme base or apex. It is not transmitted 
in any direction, as are endocardial murmurs. The friction 
sound is inconstant, coming and going without apparent 
cause, and it suffers frequent changes in character and point 
of maximum intensity. 

In cases with effusion the friction rale may disappear as 
the pericardial surfaces are separated, or the rale may be 
heard at the upper part of the heart. It reappears with the 
absorption of the fluid. On inspection there may be bulg¬ 
ing of the precordia, especially in children. The antero¬ 
lateral region of the chest may even be enlarged. Bulging 
of the precordia without visible pulsation is distinctive. 

Palpation may detect fluctuation in rare instances. The 
apex beat is usually displaced upward and outward, and the 
cardiac shock is often effaced. It is distinctive to have the 
apex beat well within the 
limits of cardiac dulness. 

The strength and location 
of the apex beat are largely 
influenced by the position of 
the patient. 

Percussion shows an in¬ 
creased area of cardiac dul¬ 
ness of a pyramidal shape, 
the apex being up, the broad 
base of the dull area produc¬ 
ing a flat note in the fifth and 
even in the sixth right inter¬ 
space. The dulness has an 

, .. 1.1 F IG - 5 -—Pericarditis with effusion, show- 

abi upt outline and extends j n g the area 0 f d u ] ne ss, the position of the 

beyond and below the apex heartwit hin the pericardial sac, and the loca- 
, ' . . tion of the apex beat (marked X)- Small 

beat. I he dulness extends crosses mark the position of the pericardial 
above the normal limits, so rales 

that very marked dulness above the third rib should 





PERICARDITIS. 


189 


lead to the suspicion of effusion. The surrounding bor¬ 
der of the lung frequently yields a tympanitic percussion 
note from its relaxation. An abundant effusion extend¬ 
ing to the left may be mistaken for pleurisy. With the 
patient in a sitting position, dulness, increased vocal frem¬ 
itus, and bronchial voice and breathing may be detected 
over a small area under the angle of the left scapula. 
These signs disappear when the patient leans forward or 
assumes the knee-chest position ; they are due to the pres¬ 
sure of an abundant effusion upon the lower lobe of the left 
lung, and they afford valuable aid to diagnosis, especially 
in children and young adults. 

On auscultation the friction rale may be heard at the base 
of the heart; the sound is inconstant, coming and going. 
It returns with the absorption of the fluid. The heart sounds 
are feeble and may become inaudible. 

Clinical Types.— 1. Latent Cases .—In these cases the 
symptoms are obscured and a diagnosis is not made during 
the life of the patient. Such cases commonly occur with 
advanced Bright’s disease. 

2. Mild Cases .—In these cases there is no appreciable 
amount of effusion and the myocardium is not involved. 
These cases give symptoms of inflammation and of slight 
derangement of the heart’s action. 

3. Severe cases are those with abundant effusion asso¬ 
ciated with myocarditis. Symptoms of inflammation and 
cardiac failure occur, and pressure-symptoms appear ac¬ 
cording to the amount of the effusion. 

4. If complicated by previous or coexisting endocarditis, 
compensation may be upset and symptoms of cardiac fail¬ 
ure with venous congestions may occur. The presence of 
these latter symptoms indicates more than mere pericar¬ 
ditis : they point always to a complicating myocarditis or 
endocarditis. 


I90 MANUAL OF THE PRACTICE OF MEDICINE . 


5. In some cases delirium, mania, or hallucinations may 
give to the disease a cerebral character. 

The diagnosis in many cases is exceedingly obscure. 
The points of diagnosis from dilated heart are concisely 
given by Sansom : 

Pericarditis. Dilatation. 


Outline of dul- 
ness. 

Rate of devel¬ 
opment of 
dulness. 

Impulse and 
apex beat. 


Relation of 
dulness to 
left apex 
beat. 

Pain over 
preco rdium 
and tender¬ 
ness in epi¬ 
gastrium. 

Pulsation in 
veins of the 
neck. 

Etiology. 


Fever. 


Dulness pear-shaped, and the 
enlargement chiefly upward. 

Often rapid and then charac¬ 
teristic. 

The impulse when present is 
in the third or fourth left 
interspace ; apex beat tilted 
upward and outward or 
effaced. 

Dulness may extend to the 
left of the left apex beat. 

Often present. 


May be present if endocardi¬ 
tis complicates. 

Usually acute, in course of 
acute rheumatism, cirrhotic 
Bright’s disease, etc. 

Often present. 


Dulness not pear-shaped, and 
enlargement chiefly down¬ 
ward. 

Usually very slow, though a 
rapid dilatation of the heart 
sometimes occurs. 

Impulse can usually be felt to 
the left of the lower end of 
the sternum or in the epi¬ 
gastrium. 

Dulness does not extend to 
the left of the left apex 
beat. 

Usually absent. 


Often present when right 
'heart is dilated. 

Usually chronic; often asso¬ 
ciated with chronic valvu¬ 
lar lesions, fatty and fibroid 
degeneration, anaemia, etc. 

Absent unless from some 
complication. 


The characteristics of the friction rale already described 
should prevent its being mistaken for endocardial murmur. 

Pleuritic frictions may be so modified by the movements 
of the neighboring heart as to resemble closely the pericar¬ 
dial rub. The pericardial friction is less liable to variation 
and is best heard when the heart is least covered by lung 
—that is, during expiration—while with the pleuro¬ 
pericardial sound the reverse is true. 








PERICARDITIS. 


I 9 I 

Pericardial effusion will not be mistaken for pleurisy with 
effusion if careful examination be made. 

The prognosis generally is good. It depends (1) upon the 
cause of the disease, being worse in distinctly septic cases 
and in old people with advanced nephritis; (2) upon the 
severity of the lesion; and (3) upon the condition of the 
heart itself—how it does its work, and whether it be the seat 
of myocarditis or of previous or complicating endocarditis. 
The prognosis of cases occurring with pneumonia is better 
than that of any other form. 

Treatment. —The patient should be put to bed and kept 
absolutely quiet mentally and bodily. The bowels should 
be opened by calomel and Epsom salt. To control the 
inflammation continuous application of cold by ice-bags or 
by Leiter’s tubes is often of the greatest service. Counter¬ 
irritation by cups, poultices, blisters, or tincture of iodine 
may be resorted to, and local blood-letting by leeches ap¬ 
plied to the precordium may be employed in robust sthenic 
cases. Small doses of opium are serviceable in steadying 
the heart and controlling the symptoms. Aconite should 
be given in case of tumultuous heart-action, to reduce the 
work of the heart to a minimum. 

Should symptoms of a failing heart appear, stimulants 
are indicated, whiskey and digitalis being the most efficient. 

To promote absorption of the effusion, blisters over the pre¬ 
cordium are recommended. The bowels should be opened 
freely, if the patient is not debilitated by over-catharsis, and 
diuretics should be given, an efficient combination being the 
infusion of digitalis with iodide and acetate of potassium. 

When the effusion is giving rise to pressure-symptoms 
and cannot be absorbed by the foregoing measures, aspira¬ 
tion may be performed. Puncture is best made in the fifth 
left interspace about two inches from the sternum—roughly, 
therefore, in the position of the normal apex beat. 


192 MANUAL OF THE PRACTICE OF MEDICINE. 

PURULENT PERICARDITIS. 

Etiology. —This form of pericarditis, which results from 
infection by the bacteria of suppuration, complicates the 
septic and pysemic diseases already alluded to as causative 
of pericarditis. The disease is frequently seen with influenza. 
Infection of a serous effusion may occur from the use of an 
infected aspirating needle. It may occur with pneumonia 
due to diplococcus infection. The tubercular form of puru¬ 
lent pericarditis will be described in a separate article. 

Pathology. —The pericardium is thickened and is infil¬ 
trated with fibrin, serum, and pus-cells ; its superficial layers, 
which are converted to granulation-tissue, may present dis¬ 
tinct ulcerations. The pericardium is usually covered with 
a thick layer of fibrin and pus. The effusion is distinctly 
purulent and is usually abundant, at times exceeding thiee 
liters. The myocardium is always more or less involved; 
it may be the seat of an acute myocarditis or of a fatty 
degeneration. 

The suppurative process may extend in any direction, so 
that the effusion may rupture into a bronchus or into the 
trachea, or may appear externally through the thoracic 
wall. In rare cases the pus may be absorbed partially, 
cheesy deposits alone remaining on the surface of the peri¬ 
cardium, which becomes thickened and may be infiltrated 
with lime salts. Should the pus be withdrawn by opera¬ 
tion, the pericardium may become thickened and adherent, 
or it may remain as a chronic suppurating surface discharg¬ 
ing its contents through a thoracic fistula. 

In long-continued cases amyloid changes occur in the 
arteries, spleen, liver, and kidneys, and chronic diffuse 

nephritis is likely to develop. 

The symptoms are generally those of serous pericarditis. 
The inflammatory symptoms are the same, but they are 
likely to be obscured by those of the original septic disease, 


CHRONIC ADHESIVE PERICARDITIS. 


*93 


so that the pericarditis may escape unnoticed. The symp¬ 
toms of mechanical pressure are identical with those of the 
serous form. Myocarditis, however, being more extensive, 
gives prominent symptoms—heart failure, rapid and feeble 
pulse, cerebral anaemia, dyspnoea, and even venous conges¬ 
tions. Septic symptoms make their appearance and indi¬ 
cate the presence of pus—erratic chills followed by sud¬ 
den rises in temperature, cold sweating, rapid and feeble 
pulse, diarrhoea, and a low form of delirium. 

The physical signs are those of pericardial effusion. 
Should pointing occur, the skin becomes red and shining 
and fluctuation may be detected. In case of doubt as to 
the nature of the effusion, hypodermic aspiration under 
antiseptic precautions should be employed. 

The prognosis is bad. The primary septic disease may of 
itself be fatal. The myocarditis is apt to lead to dangerous 
heart failure, and even if the effusion be removed by opera¬ 
tion, the pericardium never returns to a normal condition, 
and the danger of adhesive pericarditis should be con¬ 
sidered. The prognosis of cases complicating pneumonia 
is less grave than in the other forms. 

Treatment is entirely surgical. The pericardium should 
be opened freely and drained. The opening should usually 
be made in the fifth interspace, one and a half inches from 
the edge of the sternum. 

CHRONIC ADHESIVE PERICARDITIS. 

Etiology and Pathology. —Thickening of the pericardium 
and the formation of connective-tissue adhesions between 
its opposed surfaces follow dry pleurisy or the absorp¬ 
tion of the serous effusion. This condition may also follow 
absorption of a sero-purulent exudate, the pericardium being 
thickened by connective tissue covered with a cheesy 
deposit and often infiltrated with salts of lime. If the 
13 


194 MANUAL OF THE PRACTICE OF MEDICINE . 

adhesions are such as not to impede the action of the heart, 
there may be little or no change in its structure. If the 
adhesions are firm and short, the impediment afforded to 
the free action of the heart leads to hypertrophy, frequently 
of enormous dimensions. Thus compensation is estab¬ 
lished. Fatty degeneration and dilatation finally result in 
heart failure. Pleuro-pericardial adhesions are usually 
present. 

Symptoms.—As long as the heart’s power is good, 
symptoms are indefinite and may be absent. When myo¬ 
cardial degeneration and dilatation ensue, symptoms of 
failure of cardiac power result, as shown by arterial anaemia 
and venous congestions. The pulse becomes weak and 
irregular, and the pulsus paradoxus may be noted. There 
may be attacks of angina, and sudden death may occur. 
There are frequently observed recurring attacks of acute 
dry pericarditis. 

Physical Signs.—The heart is usually hypertrophied. 
It may be dilated, and there may be the systolic apical 
murmur of relative incompetence of the mitral valve. A 
significant sign is the retraction of the apex during systole. 
This sign, however, is not absolutely diagnostic, and it may 
be absent. After the systolic retraction the chest-wall may 
suddenly rebound during diastole, often with a sharp 
shock. The rapid rebounding of the chest-wall may sud¬ 
denly empty the jugular veins, giving rise to the “ diastolic 
collapse,” or Friedreich’s sign. 

The heart sounds may be normal, or muffled if the peri¬ 
cardial layers be greatly thickened. There may be distinct 
and persistent friction sounds, often of a grating, creaking, 
or “ new-leather ” character. 

The prognosis is not good. Compensation is almost cer¬ 
tain to be upset by myocardial degeneration and dilatation. 
Sudden death often occurs. 


TUBERCULAR PERICARDITIS. 


195 


Treatment consists in steady counter-irritation applied to 
the precordium, and the treatment of cardiac weakness 
when it occurs. Avoidance of severe or sudden exertion is 
to be enforced strictly. 

TUBERCULAR PERICARDITIS. 

Tuberculosis of the pericardium may be part of a general 
infection or it may be a local disease. It is of rare occur¬ 
rence, and usually results from extension from tubercular 
disease of the bronchial or mediastinal glands, the lungs, or 
the pleurae, although in many cases the primary lesion may 
be so slight as to pass unnoticed. 

Pathology. —Four forms of the lesion are seen: (1) The 
pericardium is thickened by imbedded tubercules; its sur¬ 
face is congested and covered with fibrin. (2) The peri¬ 
cardium resembles the first form, but there is an exudate of 
serum as well. (3) The pericardium is bright red and 
studded with white points, which are the tubercules. There 
is a hemorrhagic effusion. (4) The pericardium is thickened 
and infiltrated with connective-tissue cells and masses of 
tubercle-tissue ; its surface is coated with fibrin, pus, and 
broken-down tubercle-tissue. There is a purulent effusion 
often containing shreds of cheesy tissue in which the bacilli 
are to be found. 

The symptoms of tubercular pericarditis resemble those 
of the non-tubercular forms in essential features and physi¬ 
cal signs. They differ in the following particulars: (1) The 
disease is insidious, the first symptoms usually being weak¬ 
ness, loss of flesh, and anaemia. (2) The symptoms are per¬ 
sistent, without tendency to improvement. The effusion 
recurs in spite of drug-treatment or aspiration. (3) The 
course of the disease is steadily downward. Recovery is 
possible, though rare, and is not to be expected except in 
slight lesions. 


196 MANUAL OF THE PRACTICE OF MEDICINE. 

Diagnosis is aided by the absence of the ordinary causes 
of pericarditis and by the presence of tubercular lesions, 
especially within the thorax. Double pleurisy with effusion 
or with pericarditis is almost always tubercular. Hemor¬ 
rhagic effusion may occur in pericarditis of the aged or the 
scorbutic, but is much more significant of tuberculosis or of 
cancer. The finding of tubercle bacilli in the pericardial 
effusion will of course settle the diagnosis past all dispute. 

Treatment is that of the pericarditis after established prin- 
ples, and of the general condition by the supporting treat¬ 
ment that is employed in all tubercular cases. 

CANCEROUS PERICARDITIS. 

Cancer or sarcoma of the pericardium is rare and is 
almost never primary. Besides the malignant new growths 
the pericardium presents the lesions of simple inflammation 
with serous, or more frequently with hemorrhagic, exudate. 

The symptoms are those of a slowly-developing pericar¬ 
ditis with effusion. Pain is often lancinating and excessive. 
Aid is afforded in diagnosis by the hemorrhagic character 
of the effusion (as in tubercular peritonitis), the presence of 
the primary malignant growth, and the symptoms of can¬ 
cerous or sarcomatous cachexia. 

The prognosis is invariably bad. 

Treatment is merely palliative. Injections of toxic prod¬ 
ucts of erysipelas germs may be employed in sarcomatous 
cases. 

HYDROPERICARDIUM. 

Large serous effusions without inflammatory signs, 
constituting “ dropsy of the pericardium,” occur in con¬ 
nection with general dropsy, usually due to kidney or heart 
disease. 

Symptoms. —Associated with dropsical effusions in the 
pleural cavities, this condition embarrasses the action of the 


HALM 0 PERICARDIUM.—PNE UMOPERICARDIUM. 197 

heart and the lungs. The disease may occur after scarlet 
fever without general dropsy. There are no inflammatory 
symptoms. 

Physical Signs.—The physical signs are those of effusion, 
but there is no friction rale. 

ELEMOPERICARDIUM. 

Blood in the pericardium results from rupture of an 
aneurysm of the first part of the aorta, of the coronary 
arteries, or of the heart itself, from rupture of the heart-wall 
in myocarditis, or from penetrating wounds or severe crush¬ 
ing of the thorax. 

The symptoms are those of heart failure and of hemor¬ 
rhage in general. When the hemorrhage occurs slowly, 
the symptoms of heart failure may be obscured by nausea 
and vomiting. Pericarditis with bloody effusion cannot 
properly be called haemopericardium. 

The prognosis is bad. Recovery, however, may occur in 
case but little blood has been lost. 

PNEUMOPERICARDIUM. 

Air in the pericardial sac may occur from penetrating 
wounds of the chest or from perforation of the lungs, 
oesophagus, or stomach. Gas may result from the decom¬ 
position of a purulent exudate. Acute pericarditis is always 
excited, in most cases with a purulent exudation. 

The symptoms are those of cardiac failure—fever and 
pericardial effusion. Death usually follows rapidly. 

Physical Signs.—It is characteristic of pneumopericar¬ 
dium to have a movable area of dulness over the fluid, 
with an overlying area of tympany over the gas. The 
heart sounds may be distant and feeble but of a metallic 
gravity. There are splashing, churning sounds of a metal¬ 
lic quality with frictions. 


198 MANUAL OF THE PRACTICE OF MEDICINE. 

The diagnosis is to be made from dilated stomach, 
sacculated pyopneumothorax, large superficial pulmonary 
cavity, and in rare cases from hernia of intestine through a 
congenital opening in the diaphragm. 

The prognosis is almost hopeless except in recent trau¬ 
matic cases. 

Treatment consists in free incision and drainage. 


2. DISEASES OF THE HEART. 

HYPERTROPHY AND DILATATION. 

The heart is an organ with a definite function—to main¬ 
tain the circulation of the blood—and its diseases are 
important only to the extent to which they modify this 
function. The effect of all cardiac lesions is one: the heart 
is prevented from doing its work. The variety of the lesion 
is less important than its results on the power of the heart. 

There are three things to be considered in the work of a 
normal heart: (1) The heart is a hollow muscle contracting 
on its contents; (2) the heart drives the blood against 
resistance; (3) the onward flow of blood is facilitated by 
the perfect condition and action of the valves. Any one 
of these three conditions may become deranged, and so 
cause interference with the work of the heart. 

Causes Preventing the Heart from doing its Work.— 
I. Weakness of the Heart-muscle. —This weakness may 
be either comparative or actual. 

1. Comparative Weakness. —Here the heart, though 
normal in strength, is not strong enough to do an extra 
amount of work that may be required of it. This con¬ 
dition is seen in severe and sudden over-exertions , as in 
rowing-races, especially without previous training, or in 
exertion, even to a moderate extent, in high altitudes, or 



HYPERTROPHY AND DILATATION. 


I 9 9 


when the proper expansion of the chest is prevented, as by 
the heavy cross-straps of soldiers on the march, the action 
of the heart becoming secondarily embarrassed and in¬ 
sufficient to meet the demands made upon the organ. 

2. Actual weakness is the more important form, not only 
because it is continuous in its action, but also because the 
heart is rendered unfit to meet the demands of ordinary life. 
The heart-muscle may become weakened in the following 
ways: 

(a) By degeneration , either acute, as in fevers and infec¬ 
tious diseases, or chronic, as in fatty heart. 

( b ) By inflammation , either acute, as in acute myocarditis, 
which so commonly complicates pericarditis, or chronic, as 
in chronic interstitial myocarditis. 

(e) By poor nutrition. (1) In some cases the nutrition of 
the whole body suffers as well as the heart, as during con¬ 
valescence from a prolonged fever or in the case of profound 
anaemia, the heart as well as the other organs being poorly 
supplied with blood, frequently giving rise to dilatation and 
cardiac symptoms. (2) In other cases the heart alone suffers. 
This condition arises when, by reason of atheroma of the 
coronary arteries, the supply of blood to the heart-muscle 
itself is lessened. 

II. Increased Peripheral Resistance. —It is important 
to remember that increased peripheral resistance may occur 
either in the systemic vessels, interfering in consequence 
with the action of the left side of the heart, or in the pul¬ 
monary vessels, interfering with the work of the right heart. 
Each system, then, must be considered separately. 

1. Increased peripheral resistance in the systemic circula¬ 
tion , affecting the work of the left heart. 

{a) By atheroma or aneurysm of the aorta or great vessels. 

if) By endarteritis , because of the narrowed lumen and the 
non-yielding walls of the small arteries. 


200 MANUAL OF THE PRACTICE CF MEDICINE. 


(ff) By spasm of the small arteries. The spasm may occur 
as (i) the result of an endarteritis, or (2) from Bright’s 
disease, (3) uric-acid diathesis, (4) gout, (5) diabetes, or (6) 
over-eating and excessive drinking. 

2. Increased peripheral resistance to the pulmonary circu¬ 
lation, affecting the work of the right heart. 

(a) By failure of the left heart , either from its muscular 
weakness, from dilatation, or from valvular disease, espe¬ 
cially lesions of the mitral valve. 

iff) By obstruction of the pulmonary vessels by spasm, 
endarteritis, or obliteration. This condition occurs in em¬ 
physema, in interstitial pneumonia, and to some extent in 
pulmonary phthisis. 

III. Error in the Valves. — 1. By stenosis of any valve, 
the valve-orifice becoming narrowed, there is difficulty in 
the onward passage of the blood. 

2. By insufficiency of any valve, so that blood can regur¬ 
gitate backward instead of being prevented from so doing 
by perfect closure of the valve. 

Valvular insufficiency may result in one of four ways : 

(<7) By inflammation , causing thickening and contraction 
of the valve. 

(b) By rupture from violence or from ulceration. 

iff) By stretching of the orifice to which the valve-segments 
are attached. This applies especially to the mitral valve. 
The mitral-valve segments can close the left auriculo-ven- 
tricular orifice, provided it be of normal size; but should 
the left ventricle become dilated, the auriculo-ventricular 
orifice becomes stretched to too great a size to be covered 
by the valve-segments during their closure, hence regurgi¬ 
tation of blood is permitted at the time of the ventricular 
systole. This condition is often spoken of as “ relative 
incompetence.” 

Regurgitation into the left ventricle may occur at the 


HYPERTROPHY AND DILATATION. 201 

time of the ventricular diastole, past the aortic valve if the 
aortic ring be stretched by an aneurysm of the aorta near 
the valves, even if the latter be normal. 

(d) By poor ventricular contraction. The relation of mus¬ 
cular fibres to the mitral ring is such that when the fibies 
contract the auriculo-ventncular orifice is reduced to one- 
half its size and can then be covered by the normal valve- 
segments. If the contraction be poor, the orifice is not so 
much diminished in size, and cannot be closed entirely by 
the valve-segments. In this way regurgitation of blood 
past the mitral valve is permitted at the time of ventricular 
contraction. T o this condition the name of relative in¬ 
competence ” is also applied. 

Methods of Compensation— When an extra amount of 
work is required ot the heart in any of the above-mentioned 
ways, the great and important question is whether the heait 
can rise to the emergency and meet the demand for the 
extra amount of work. When the increased power of the 
heart becomes equal to the increased demand, then the cir¬ 
culation is again in an equilibrium and “ compensation ” is 
established. Upon the question of compensation the whole 
prognosis and treatment of cardiac diseases depend. Com¬ 
pensation occurs in two ways : 

i. By increase of the force andfrequency of the heart s action. 
This is the simplest form of compensation, and is especially 
adapted to meet sudden demands. The rapid and forcible 
heart’s action after a short run is the best example that can 
be cited. Compensation by increase of the heart’s action is 
often associated with hypertrophy, and it is most important 
that this fact be remembered. For example, in aortic 
regurgitation hypertrophy of the left ventricle is hardly 
efficient enough by itself to compensate for the diastolic 
regurgitation of blood. There must also be an increased 
frequency of ventricular contraction to keep the ventricle 


202 MANUAL OF THE PRACTICE OF MEDICINE . 

emptied of the blood which, during diastole, pours into it 
not only from the auricle, but backward as well from the 
aorta, past the inefficient aortic valve. It is poor practice to 
try to reduce the pulse-rate of such a case to the normal 
limit of 72 to the minute. If we do, we run the risk of giv¬ 
ing the ventricle time enough between contractions to be¬ 
come distended to too great a limit, with disastrous results. 

2. By hypertrophy. 


Hypertrophy. 

Hypertrophy is an actual increase in the amount of 
cardiac muscle, giving the heart thereby increased force 
adequate to the increased demand for force. The condition 
is purely compensatory and physiological, and is analogous 
to the enlargement of the biceps of a blacksmith. Certain 
conditions must be complied with before hypertrophy can 
occur. 

1. A certain amount of time is necessary. Hypertrophy 
is a slow process, requiring a minimum time of two weeks 
for its development. Preceding its completion there may 
be a primary compensation by increased force and fre¬ 
quency of the heart’s action. The process of hypertrophy 
is so slow that patients may die from disturbed circulation 
before compensation is established. 

2. The lesion must not be excessive. It can readily be seen 
that in very extensive lesions no amount of muscular 
hypertrophy can restore the circulation to an equilibrium. 

3. The lesion must not be too rapidly progressive. A lesion 
slight at first may be perfectly compensated, but if it pro¬ 
gresses it may become too severe for hypertrophy to keep 
up with it. 

4. There must be a healthy condition of the heart-muscle. 
This is of the utmost importance. Weakness of the heart- 
muscle may prevent hypertrophy entirely or may only allow 


HYPERTROPHY AND DILATATION. 203 

a degree of hypertrophy inadequate to the demand, so that 
compensation occurs but imperfectly. Weakness of the 
heart-muscle may at any time prevent the maintenance of 
hypertrophy, so that compensation will fail. The treatment 
of a hypertrophied heart consists solely in the maintenance 
of a proper amount of hypertrophy, and this state depends 
in the greatest degree upon the condition of the heart-mus¬ 
cle itself. It is important, then, to consider in what ways 
the heart-muscle may be weakened. 

Local Causes .— (i) Degeneration , either fatty, fibroid, or 
the acute degeneration of fevers; (2) inflammation as 
complicating acute endocarditis or pericarditis; (3) poor 
blood-supply , from atheroma of the coronary artery or from 
severe general anaemia. 

General Causes. —(1) General weakness and debility; 
(2) old age; (3) anaemia; (4) lack of proper care of self; 
indulgence in alcohol and tobacco, irregular hours and 
habits, exhausting work, improper food, etc. 

Symptoms of Hypertrophy.—If there be compensatory 
hypertrophy adequate to meet the extra demand on the 
heart, the circulation will be in perfect equilibrium and there 
will be no subjective symptoms. The diagnosis is made by 
the finding of some cause demanding the performance of 
extra work. This cause may be valvular error or increased 
peripheral resistance from endarteritis or from the arterial 
spasm of Bright’s disease, or from any of the other men¬ 
tioned causes, but in all cases alike perfect compensation 
allows of no circulatory disturbances. 

Physical Signs of Hypertrophy of the Left Side of the 
Heart.— Inspection may show some bulging of the pre- 
cordia, especially in children, in whom asymmetry of the 
chest may become apparent. The area of visible impulse 
is much increased, and the apex beat is seen to be displaced 
downward and outward. 


204 MANUAL OF THE PRACTICE OF MEDICINE. 


Palpation .—There occurs over the lower part of the heart 
a slow, heaving impulse which is one of the most distinctive 
signs of simple hypertrophy. The apex beat occurs as a 
powerful, deliberate thrust, and is felt downward and out¬ 
ward from its normal situation. It may be felt in the sixth, 
seventh, or eighth intercostal space and outside the nipple 
line. The position of the apex beat is a good guide to the 
position of the left border as found by auscultatory percus¬ 
sion. If the apex beat be continuously strong and heaving, 
it proves a healthy condition of the myocardium and is of 
good prognostic value. The character of the apex beat aids 
in differentiating hypertrophy from dilatation. In some 
patients with deep, well-covered chests, and in those whose 
lungs are emphysematous, overlapping the heart to an ab¬ 
normal degree, the signs by inspection and palpation may 
not be apparent. 

Percussion should by preference be performed by the aus¬ 
cultatory method, as greater accuracy is thereby assured. 
There is increase in the transverse area of dulness, so that 
the left border lies distinctly outside the nipple line. A 
transverse diameter of over four and a half inches is never 
seen in a normal heart. In some cases the transverse 
diameter is not increased by percussion, so that the 
diagnosis must be made by other signs. There is also 
an increase in the vertical direction, the upper limit of 
cardiac dulness being frequently in the second intercostal 
space. 

Auscultation .—In hypertrophy without valvular disease the 
sounds of the heart may be normal, or the first sound at the 
apex may be prolonged and of a booming, muscular quality. 
Reduplication is common in the hypertrophy consequent 
upon kidney disease. The second sound heard over the aortic 
area is loud, clear, and snappy, being “ accentuated.” This ac¬ 
centuation of the second aortic sound is heard best in hyper- 


HYPERTROPHY AND DILATATION. 


205 


trophy consequent upon increased arterial resistance. For 
its development there must be not only increased resistance 
in front, but also increased force from behind, so that at each 
systole blood is pumped into the aorta with force enough to 
give rise to tension high enough to overcome the increased 
peripheral resistance. The accentuation is due to the forcible 
closure of the aortic valves at the beginning of diastole by 
reason of this high arterial pressure. The very presence of 
an accentuation of the second aortic sound is of good 
prognostic significance, as it proves necessarily that the 
heart is able to do its extra work. The disappearance of 
the accentuation and the weakening of the second aortic 
sound imply weakening of the heart’s power, and are of 
bad import. 

In hypertrophy dependent upon valvular lesions the heart 
sounds are necessarily altered and are replaced or associated 
with murmurs. 

In hypertrophy associated with dilatation the physical 
signs are correspondingly modified. 



Fig. 6.—Sphygmogram showing high tension in Bright’s hypertrophy. 


The pulse of hypertrophy not due to valvular disease is 
full, strong, and of high tension. Its characteristics are 
best seen in cases of hypertrophy consequent upon in¬ 
creased peripheral resistance, as endarteritis in Bright s 

disease. 

Physical Signs of Hypertrophy of the Right Side of the 
Heart. —Inspection may reveal bulging of the lower part 
of the sternum. Below the ensiform cartilage there is a 





























206 manual of the practice of medicine . 


visible pulsation due to the enlargement downward of the 
hypertrophied right ventricle. 

Palpation. —There is a distinct heaving impulse appre¬ 
ciable just below the ensiform cartilage. This epigastric 
pulsation is seen and felt also in displacement of the heart 
downward from aneurysm, from mediastinal tumors, and 
from emphysema, so that the diagnosis of hypertrophy of 
the right ventricle should always be corroborated by other 
signs. The second sound heard over the pulmonary area 
(second space to the left of the sternum) is accentuated on ac¬ 
count of increased tension within the pulmonary artery. This 
sign is of good prognostic value. The diagnosis is aided 
by the finding of the cause for the hypertrophy either in a 
failing left ventricle or in some condition causing increased 
resistance in the pulmonary circulation. 

Dilatation. 

Dilatation is reached whenever the ventricle does not 
empty itself during the systole. There are two principal 
causes of dilatation : 

1. Increased blood-pressnre within the cardiac cavities , from 
increased peripheral resistance, from valvular disease, or 
from excessive muscular effort. An extra amount of work 
is thrown on the heart, which fails to respond by hyper¬ 
trophy, either by reason of a too sudden, too extensive, or 
too rapidly progressive lesion, or by reason of impaired 
vitality of the cardiac muscle. 

2. Impaired nutrition of the heart-walls may so weaken 
their resisting power that dilatation occurs even if the heart 
be not called upon for extra work. The condition is often 
spoken of as “ idiopathic dilatation.” The result in either 
case is the same : the heart can no longer do its zvork. Three 
conditions necessarily result: (i) The arteries are underfilled 
with blood—arterial anaemia. (2) The veins are overfilled, 


HYPERTROPHY AND DILATATION . 


207 


and there are venous congestions of the various viscera that 
may be acute or may become chronic. (3) The heart can¬ 
not empty itself completely at each systole, either from too 
much work required or from deficient contraction-force, so 
that there is always a certain amount of residual blood 
which increases the size of the cardiac cavities and dilates 
them, especially if the cardiac muscle be weak and de¬ 
generate. 

Hypertrophy is a compensatory process; dilatation is 
destructive. Hypertrophy is an evidence of vigor; dilata¬ 
tion is an evidence of weakness. In hypertrophy the work 
of the heart is well done; in dilatation the work is imper¬ 
fectly performed. 

Dilatation may occur by itself or may be associated with 
hypertrophy. In some cases hypertrophy may precede, 
compensating for some pre-existing lesion; then compensa¬ 
tion fails and dilatation gradually ensues. In other cases, 
from a sudden lesion the heart is at first dilated, compen¬ 
satory hypertrophy occurring after a time. 

Symptoms.—If the left ventricle dilates, its walls 
become weakened and thinned and the mitral ring becomes 
stretched. From both of these reasons, as previously 
explained, there is apt to be developed “ relative incompe¬ 
tence of the mitral valve,” the blood being regurgitated at 
the time of the ventricular svstole into the auricle, and so 
exerting a back pressure and congestion in the pulmonary 
vessels. If the right ventricle be strong and of good 
nutrition, it will act forcibly and will hypertrophy, forcing 
the blood well into the pulmonary blood-vessels against 
this backward pressure, standing thus as a barrier between 
the dilated left ventricle and the systemic venous system. 
If, on the contrary, the right ventricle be not strong 
enough to overcome the backward pulmonary pressure and 
to sustain the circulation of blood in the lungs, the ven- 


208 manual of the practice of medicine. 


tricle will dilate, its contraction-force will be weakened, there 
will be back pressure of blood in the veins of the body, 
and general venous congestion of the viscera will ensue. 

The consideration, therefore, of the symptoms of dilata¬ 
tion is largely that of venous congestions. 

Acute Venous Congestions. — Brain .—The pia mater is 
congested and cedematous. There is an increase in the 
cerebro-spinal fluid. Clinically there are developed delirium 
with delusions, insomnia, stupor, and headaches. 

Lungs .—Congestion and oedema exist, especially marked 
posteriorly at both bases. There may be areas of hypo¬ 
static pneumonia. Clinically there is developed dyspnoea, 
at first only on exertion, later becoming steady and of the 
variety known as “ orthopnoea.” There is a cough with 
expectoration which may contain blood. The expectora¬ 
tion may be serous and profuse. On physical examination 
are found moist bronchial rales and crepitations, either 
general or at the bases alone, and there may be the physi¬ 
cal signs of consolidation in case of hypostatic pneumonia. 

Pleura .—There is hydrothorax. This gives rise to 
symptoms due to the mechanical presence of the fluid— 
dyspnoea, cough, and the displacement of neighboring 
viscera. There are the physical signs of fluid in both 
pleural cavities. 

Stomach .—There is congestion of the gastric mucosa, 
giving rise to vomiting, to occasional small hemorrhages, 
and to symptoms of gastric indigestion. 

Intestines .—There is either diarrhoea or constipation and 
a decided loss of general nutrition. 

Liver .—There are congestion, an enlargement which is 
slight and symmetrical, symptoms of disturbances in the 
functions of the liver, and frequently slight jaundice. 

Spleen .—There is moderate enlargement. 

Peritoneum .—There is a serous peritoneal effusion known 


HYPERTROPHY AND DILATATION. 


209 


as “ascites,” with enlargement of the abdomen ; mechanical 
symptoms of the effusion and the physical signs of its 
presence also exist. 

Kidneys .—The kidneys are enlarged and congested. The 
urine is diminished; albumin and casts are present in 
moderate amounts. A practical rule is that whenever the 
urine is turbid and deposits urates day after day irrespec¬ 
tive of diet, mode of life, or exercise, a failing heart should 
be looked for. 

Skin .—Cyanosis appears; there is also oedema, at first 
appearing in the feet and ankles after standing, but later 
becoming general. 

Chronic Venous Congestions. — Brain .—The pia mater 
is congested and cedematous, and the fluid in the ventricles 
is increased—the so-called “ wet brain.” There is apt to be 
considerable atrophy of the cerebral cortex. Clinically 
there are headache, attacks of dizziness, black specks before 
the eyes, buzzing noises in the ears, insomnia or unnatural 
stupor, and delirium with delusions. 

Lungs .—There is a chronic bronchitis with cough and 
expectoration. There may be repeated small hemorrhages. 
Dyspnoea is present at first on exertion, but later becomes 
steady and of the orthopnceic variety. In chronic cases 
there is developed the chronic congestion of the lung known 
as the “ pneumonia of heart disease,” or “ pigment ” or “ brown 
induration.” The lung is dry and leathery and is mottled 
brown and salmon pink in color. Microscopic examination 
shows dilatation and lengthening of the capillaries in the 
alveolar wall, so that by their loopings they encroach upon 
the air-spaces. The alveolar wall is thickened by the growth 
of its capillaries and by that of muscular fibres and new 
connective tissue. In the walls of the alveoli and in their 
endothelial cells there is a deposit of pigment due to small 
punctate hemorrhages from the congested and tortuous 
14 


210 MANUAL OF THE PRACTICE OF MEDICINE. 


capillaries. The endothelial cells are increased in number, 
in some places so filling the cavity of the alveoli as to form 
patches of hepatization. 

Pleura .—There is fluid in both pleural cavities, giving rise 
to mechanical symptoms and physical signs. 

Stomach and Intestines .—There is either chronic conges¬ 
tion or a chronic catarrhal inflammation, giving rise to 
characteristic symptoms. 

Liver .—There is the so-called “ nutmeg liver,” its name 
arising not from any surface irregularity, but from the mot¬ 
tled color. The liver may be large or small or normal in 
size. The centre of each acinus is pigmented and depressed ; 
the periphery is yellowish from fatty degeneration of the 
liver-cells. There may be a catarrhal inflammation of the 
bile-ducts with jaundice; there may also be an associated 
cirrhosis. 

Peritoneum .—There is ascites. 

Kidneys .—There may be either chronic congestion or 
chronic diffuse nephritis. In the former case the urine is 
diminished, of increased specific gravity, and may contain 
a little albumin. The quantity of urea is normal. There 
are no characteristic clinical symptoms. In the case of 
chronic diffuse nephritis the urine, which may be either 
diminished or increased in quantity, contains a diminished 
amount of urea. There may or may not be albumin and 
casts. The specific gravity of the urine is regularly low, be¬ 
ing about 1010. This form of nephritis is apt to give 
symptoms of chronic ursemia. 

The occurrence of nephritis with cardiac dilatation is not 
always the same. 

I. In some cases the dilatation begins first from valvular 
disease or from any other cause giving rise to venous con¬ 
gestions, including congestion of the kidney, which develops 
into chronic diffuse nephritis. 


HYPERTROPHY AND DILATATION. 


21 I 


2. In some cases there is first developed a chronic diffuse 
nephritis, by reason of which toxic products, not being 
properly excreted, collect in the blood, causing endarteritis 
and arterial spasms. This condition increases peripheral 
resistance, which is met by hypertrophy of the left ventricle. 
Should this compensation fail, there will be added dilata¬ 
tion of the heart. 

3. In other cases hypertrophy with subsequent dilatation 
and chronic diffuse nephritis occurs as part of the disease 
process known as “ arterio-capillary fibrosis.” 

Skin .—There may be cyanosis. There is a characteristic 
obliteration of the fine lines and wrinkles of the skin of the 
face, due to its congestion and moderate oedema. There is 
oedema, first noticed in the ankles on walking or standing, 
later becoming more generally distributed. 

Physical Signs of Dilatation.— t. Of Dilatation of the 
Left Heart.—Inspection shows a diffuse undulatory pulsa¬ 
tion over a large area. There may be, however, no pulsa¬ 
tion visible. 

Palpation .—The impulse is vibratory and diffused. There 
are cases in which the pulsation can be seen but cannot be 
felt. The apex beat is poorly defined; it is diffused, weak, 
snappy, or absent. 

Percussion .—There is enlargement of cardiac dulness both 
vertically and transversely. The left border of the area of 
dulness is frequently found as far as the anterior axillary 
line. The upper border may be at the second rib ; the apex 
may be carried downward as far as the seventh or eighth 
rib. The increase of size is in the same direction as in 
hypertrophy, but is carried to a greater extent. 

Auscultation .—The first sound at the apex is short and 
snappy, approaching the character of the more purely valv¬ 
ular second sound. The second sound at the base is weak 
or absent. Both of these signs are important in making a 


212 MANUAL OF THE PRACTICE OF MEDICINE. 

diagnosis between dilatation and hypertrophy. In some 
cases the first and second sounds are alike and equidistant, 
showing a short, ill-sustained systole. This is a serious sign, 
and it is spoken of as “ embryocardia.” In many cases the 
first sound is replaced by the murmur of relative incompe¬ 
tence of the mitral valve. Diagnosis is often impossible 
between idiopathic dilatation with relative mitral incompe¬ 
tence and mitral regurgitation with consequent dilatation. 
The murmur of mitral stenosis is apt to disappear if dila¬ 
tation be established. The pulse of dilatation is weak, 
irregular, and of low tension. It goes to pieces after any 
physical exertion. 

If the right ventricle be in good condition, it will hyper¬ 
trophy, giving the physical signs of this condition. Espe¬ 
cially important is the presence of an accentuated second 
pulmonary sound and the absence of general venous con¬ 
gestion. 

2. Of Dilatation of the Right Heart .—If the right ventricle 
dilate, it will become more enlarged to the right and 
downward, giving rise to a wavy impulse under the ensi- 
form cartilage and frequently in the six and seventh 
spaces to the left of the sternum. The accentuated second 
pulmonary sound is replaced by a weak or absent second 
sound, and symptoms of venous congestions make their 
appearance. If the dilatation be extreme, there may be 
relative incompetence of the tricuspid valve with pulsations 
of the liver and the jugular veins. 

ACUTE ENDOCARDITIS. 

Theoretically any part of the endocardium may be the 
seat of inflammation, but practically the endothelium of the 
valves and of their immediate vicinity is affected. In post¬ 
natal endocarditis the right heart is but seldom involved 
except in malignant cases. Figures 7-10 show endarteritis 


ACUTE ENDOCARDITIS. 21 3 

and the successive stages of compensation (hypertrophy) 
and of failing compensation (dilatation). 



Fig. 7.—Diagram showing normal condition of circulation. 



Fig. 8.—Diagram showing compensatory hypertrophy of the left ventricle following 

endarteritis; right heart normal. 



Fig. 9.—Diagram showing failure and dilatation of the left ventricle (failing compensa¬ 
tion), stretching of the mitral ring allowing mitral regurgitation, with hypertrophy of the 
right ventricle (compensatory); some pulmonary congestion, no general venous congestion. 



Fig. 10.—Diagram showing total failure of compensation ; the right ventricle is dilated ; 
tricuspid leakage occurs; there are both pulmonary and general venous congestions. 

Etiology. —Endocarditis does not occur as a primary 
disease, but always occurs in association with other affec- 


























214 MANUAL OF THE PRACTICE OF MEDICINE. 

tions. The affection may be produced artificially by the 
injection into the blood of various pathogenic micro-organ¬ 
isms, especially if the valves be injured or be the seat of 
chronic inflammation. The view that endocarditis is a 
disease of bacterial infection is becoming more and more 
prevalent. The most important cause is acute articular 
rheumatism, from 60 to 85 per cent, of all cases being 
due to this disease. Endocarditis may complicate the 
abarticular form of rheumatism in children, in which case 
the primary cause is often overlooked. According to 
Osier, endocarditis commonly follows chorea: “ There is no 
disease in which post-mortem acute endocarditis has so 
frequently been found.” The disease complicates the 
exanthemata, especially scarlet fever. It may accompany 
any septic or infectous disease. It has thus been found with 
pneumonia, erythema, gonorrhoea, dysentery, pyaemia, and 
puerperal fever. Suppurative infectious diseases, however, 
are more commonly the cause of the malignant form. In 
ulcerative processes such as phthisis, typhoid fever, or 
ulcerating carcinomata, slight inflammations of the endothe¬ 
lium are frequently found ; these have, however, as a rule, 
no clinical interest. 

Pathology.—The endocardium is a connective-tissue 
membrane covered with epithelium and poorly supplied 
with blood-vessels, hence its inflammations are of the 
cellular rather than of the exudative variety. There are 
three grades of severity: (1) There is a simple swelling of 
the valve-segments, their surface being smooth. (2) There 
is swelling of the valves with a new cell-growth in places, 
so that the surface is covered by vegetations composed of 
granulation-tissue capped with fibrin. There may be found 
in the vegetations bacteria of various kinds, but their 
relation to the disease process is not known. The vegeta¬ 
tions occur on the valve-segments at their lines of maxi- 


A CUTE END O CA EDIT/S. 


215 


mum contact when closed. (3) The cell-growth may be so 
excessive that the cells undergo necrosis, causing ulceration 
or perforation of the valve. This condition is more 
common in the malignant form. The mitral valve is the 
one most frequently affected, next the mitral and the aortic, 
more rarely the aortic valve alone. 

Effects of the Lesion.—1. The diseased valve is ren¬ 
dered incompetent from stenosis, from insufficiency, or from 
both. 

2. The inflammation may extend to the myocardium, so 
that it is infiltrated with cells. This inflammation is rarely 
severe, but it tends to weaken materially the power of the 
heart. 

3. Pieces of vegetations may become detached, enter the 
blood-current, and lodge in peripheral arteries, causing 
embolism. The emboli are non-infective in simple endo¬ 
carditis. 

4. In many cases—estimated as one-third by some 
authors—pericarditis occurs, both diseases arising from a 
common etiology. Extension of inflammation to the peri¬ 
cardium through the myocardium has occurred, but is 
exceedingly rare. 

5. Acute endocarditis frequently attacks a heart that is 
the seat of a chronic endocarditis, this condition predispos¬ 
ing toward a new infection, and may thus upset compensation. 

6. In acute cases it does not make very much difference 
which valve is affected. The chief question is, How does 
it affect the work of the heart? As the lesion is sudden, 
compensation at first is only by increase of frequency and 
possibly by increase of force; later comes the question of 
hypertrophy. 

Symptoms. —The symptoms may be divided into three 
groups: 1. Symptoms of inflammation; 2. Symptoms of 
valvular insufficiency; 3. Symptoms of embolism. 


21 6 MANUAL OF THE PRACTICE OF MEDICINE. 


1. Symptoms of Inflammation. —There may rarely be an 
initial chill. The temperature in almost all cases becomes 
elevated; it may be 104° or 105° in children, but is rarely 
as high in adults; it is often irregular. 

In the majority of cases (75 per cent.) there are peculiar 
feelings referred to the heart. The patient complains of 
vague precordial distress, a sense of heaviness, a feeling as 
if the heart were being squeezed, etc. Actual pain is rare. 
When it does occur, it is apt to resemble angina and may 
be referred to the epigastrium. The inflammatory symp¬ 
toms may be obscured by those of the disease to which the 
endocarditis is secondary. 

2. Symptoms of Valvular Insufficiency. — Ihe breathing is 
rapid, and usually there is subjective dyspnoea. If the 
myocardium be not involved, the pulse is rapid and the 
heart’s action is tumbling and tumultuous from compensa¬ 
tory over-action. There is the subjective feeling ol palpita¬ 
tion. If there be myocarditis, the pulse becomes rapid and 
feeble. There are symptoms of arterial anaemia—faintness, 
syncope, small feeble pulse, and spots before the eyes. 
There may be symptoms of any of the venous congestions 
mentioned under “ dilatation,” depending on the severity 
and extent of the lesion. 

3. Symptoms of embolism may arise at any time. Sudden 
lumbar pain accompanied with albuminuria or haematuria 
indicates embolism of the kidney. Pain and swelling of the 
spleen indicate embolism of that organ. Fhnbolism of the 
brain is recognized by various paralyses depending upon 
the location of the embolus, and by disturbances of con¬ 
sciousness. Embolism of the lungs occurs only with 
endocarditis of the right heart. 

Physical Signs. —The most common physical sign is a 
“bellows murmur,” systolic, heard best at the apex and 
transmitted to the left, although imperfectly. This sign is 



Acute endocarditis following defervescence of acute articular rheumatism, showing temperature (black), pulse (red), and respirations (blue). 





































































































































































































































































































I 









A CUTE END OCA RDIT1S. 


217 


generated by mitral insufficiency. Other murmurs may be 
heard according to the valve affected, but diastolic mur¬ 
murs are rare. The rhythm of the murmur is often hard 
to determine, from the tumultuous action of the heart. 
The presence of a murmur alone is not diagnostic, and 
there are cases without murmurs. The association of an 
over-acting tumultuous heart and a small feeble pulse is of 
some diagnostic valve. There may be the physical signs 
of dilatation of the left ventricle with accentuation of the 
second pulmonary sound. There may be added the 
physical signs of venous congestion. 

Course of the Disease.— i. Latent Cases .—The lesion is 
slight and is perfectly compensated. There are no symp¬ 
toms. Physical signs may be present. In some of these 
cases the valve may return to a normal condition. Em¬ 
bolism may occur, however mild the case. 

2. Mild Cases .—There are present inflammatory symp¬ 
toms, but the circulation is not disturbed and there are no 
symptoms of valvular inefficiency. In severer cases there 
may be a tumultuous action of the heart and some 
dyspnoea. 

3. Severe eases result either from an extensive lesion, 
from a secondary myocarditis preventing compensation, or 
from an acute endocarditis engrafted upon a chronic pro¬ 
cess, upsetting compensation. Very rarely there may be 
sudden death from excessive circulatory derangement. 
There are developed symptoms of pulmonary congestion. 
If the right ventricle hold good, there will be no general 
venous congestions. These, however, will occur if the 
risfht ventricle fail in its work. 

o 

Prognosis. —Acute endocarditis rarely proves fatal 
unless complicated by severe pericarditis or myocarditis. 
A few cases with healthy valves recover, especially those 
cases secondary to chorea. The liability to organic valvu- 


218 manual of the practice of medicine. 


lar changes is great. The possibility of repeated attacks, 
especially in rheumatic cases, must be taken into considera¬ 
tion. An acute attack engrafted upon a chronic endocardi¬ 
tis may upset compensation and lead to a fatal dilatation. 
Sudden death is exceedingly rare. The occurrence of 
embolism adds an uncertain element to every case. 

Treatment.—The old idea that endocarditis could be 
prevented by curing rheumatism early has not been sus¬ 
tained. Still, it is best to treat every case of rheumatism 
and chorea energetically from the very start. Patients with 
rheumatism should have every source of heart strain 
removed by as nearly absolute a rest as possible. This 
does not lessen the patient’s liability to have endocarditis, 
but if it does occur it is much more apt to be less severe, 
less extensive, and less permanent in its results. 

When endocarditis is once established, care should be 
taken not to depress the heart by too large doses of the 
salicylates. 

Inflammatory symptoms are best treated by strict bodily 
and mental rest, applications of cold to the heart, and small 
doses of opium. 

The action of the heart should be controlled. Stimulants 
should be given if indicated. Over-action of the heart may 
be treated by small doses of aconite or of iodide of potas¬ 
sium, or by the use of cold to the precordia. The bowels 
should be opened freely, and distention of the stomach is to 
be avoided. 

Venous congestions should be treated by heart stimu¬ 
lants and by depletion by diuretics, diaphoretics, and 
cathartics. Blood-letting may be employed in selected 
cases. 

The treatment of convalescence must be tonic and sup¬ 
porting, in order that compensation may be made per¬ 
manent. 


MALIGNANT ENDOCARDITIS. 


219 


MALIGNANT ENDOCARDITIS. 

Synonyms. —Septic, Ulcerative, Diphtheritic, Bacterial, 
Mycotic endocarditis; Arterial pyaemia. 

Etiology. —T he disease is secondary to a number of 
septic conditions: (1) It may follow puerperal fever or any 
septic condition of the puerperal state. (2) It follows septic 
wounds. (3) It may complicate certain septic diseases. Of 
these diseases, pneumonia is perhaps the most common. 
Cases have followed suppurative phlebitis from ear disease, 
erysipelas, diphtheria, suppurative pylephlebitis, osteomye¬ 
litis, dysentery, abscesses, and gonorrhoea. (4) In some 
cases no apparent cause can be found, but it is supposed 
that germ infection occurs through unnoticed cracks or 
abrasions of the skin or the mucous membranes. 

The exciting cause of malignant endocarditis is infection 
of the endocardium by bacteria. There are a variety of mi¬ 
cro-organisms capable of causing this infection, the common¬ 
est being the cocci of suppuration, the coccus of erysipelas, 
and the pneumococcus. Infection of the endocardium by 
bacteria is favored by its previous weakness or inflamma¬ 
tion, three-quarters of all cases of endocarditis occurring in 
hearts previously affected with chronic valvular disease. 

Lesion.—The lesion consists in abundant cell-growth of 
the endocardium, forming vegetations capped with fibrin, 
the base consisting of granulation-tissue; these vegetations 
contain colonies of bacteria. The cells are apt to become 
necrotic, so that by their death there are formed ulcers 
which may perforate or erode the valve-segments, the sep¬ 
tum, or even the heart itself, or which may so weaken the 
resisting power of the valve that it may become bulged, 
forming a little aneurysm. There may be infection of the 
deeper endocardial layers, with the production of small 
abscesses. 


220 MANUAL OF THE PRACTICE OF MEDICINE. 

Portions of vegetations containing bacteria are apt to be¬ 
come detached, enter the blood-current, and become emboli 
of a distinctly infective character. In this way distinct sec¬ 
ondary lesions are developed, (i) There maybe purulent 
inflammation of any of the serous membranes, meningitis, 
pericarditis, empyema, peritonitis, or suppurative inflamma¬ 
tion of the joints. (2) There may be suppurative infarctions 
and abscesses of any part of the body, especially of the brain, 
lungs, kidney, spleen, and liver. (3) There may be subcuta¬ 
neous hemorrhages from destruction of the wall of a cuta¬ 
neous blood-vessel by an infective embolus. Ptomaines 
arising from the growth of the bacteria poison the general 
system and produce the symptoms of septicaemia. 

The location of the inflammation is more widespread in 
malignant than in simple endocarditis, the right heart and 
the endocardium lining the heart-cavities being more fre¬ 
quently affected. In 209 cases the aortic and mitral valves 
together were affected in 41 ; the aortic valves alone, in 53 ; 
the mitral valve alone, in 77; the tricuspid valves, in 19; 
the pulmonary valves, in 15 ; the heart-wall, in 33; the right 
heart alone, in 9. When the endocardium lining the heart- 
cavities is affected, the most frequent situations are the upper 
part of the septum of the left ventricle and the postero-ex- 
ternal wall of the left auricle. The spleen is large and soft. 
The cells of the kidneys and the liver show degenerative 
changes. 

Symptoms.—The symptoms may conveniently be divided 
into three principal groups : 

1. Symptoms of a Sudden and Severe Heart-lesion .—The 
symptoms of this group resemble those of simple endo¬ 
carditis, but are much more sudden and severe. There are 
marked disturbances of circulation, as shown by venous 
congestion in both the pulmonary and the systemic circu¬ 
lation. The lesion, as a rule, is too sudden and severe to 


MALIGNANT ENDOCARDITIS. 


221 


allow of any approach to compensation. There are usually 
murmurs heard according to the valve affected. Diastolic 
and right-heart murmurs are more common than in simple 
endocarditis. The action of the heart is often so irregular 
and tumultuous that the rhythm of the murmurs cannot be 
determined. In some cases, especially when the lesion is 
located in the ventricular endocardium, there may be no 
murmur at all. In three-fourths of the cases there are 
present the physical signs of antecedent valvular disease. 
The size of the heart is not increased in acute cases, as the 
patient is apt to die of sepsis before dilatation can become 
appreciable; but in subacute cases dilatation may become 
evident and there may be an approach to a compensatory 
hypertrophy. 

2. Symptoms of Sepsis .—There is a decided tendency for 
the patient to pass into the “ typhoid state.” There is a 
fever which is either steady or interrupted by marked re¬ 
missions. There are frequent chills followed by sudden 
elevation of temperature, its decline being accompanied by 
sweating and prostration. Repeated erratic chills indicate 
septic material in circulation, and they should always cause 
a diligent search to be made for a septic focus in some part 
of the body. It should be remembered, however, that 
patients walking about in a condition of fever are apt to 
complain of chilly feelings. The chills of suppuration are 
too erratic to be confounded with those of malarial infection. 

3. Symptoms of Infective Emboli .—Embolic symptoms give 
different clinical features according to their localization. 
Emboli of the brain will produce paralyses of various mus¬ 
cles according to the situation of the embolus, with disturb¬ 
ance of consciousness. There may be abscess of the brain 
or meningitis, usually associated with furious delirium. In 
the lungs there may be a septic pneumonia or an abscess. 
There may be empyema. The spleen may become large 


< 


222 MANUAL OF THE PRACTICE OF MEDICINE . 

and tender and may be the seat of abscesses. Abscesses in 
the liver are accompanied by their usual symptoms. Em¬ 
bolism of the kidneys is marked by lumbar pain, by hema¬ 
turia, and possibly by the presence of pus in the urine. 
Petechial rashes may resemble the eruption of certain cases 
of typhoid or of cerebro-spinal meningitis. In some cases, if 
associated with multiple skin abscesses, the appearance of 
the patient may be suggestive of hemorrhagic small-pox. 

The diagnosis of malignant endocarditis is made by the 
combination of the three groups of symptoms. Any one 
group, however, may be slight or even latent, and any one 
group may predominate and give its stamp to the disease. 

(1) If the symptoms of the heart-lesion predominate, the 
case will resemble simple endocarditis or chronic endocar¬ 
ditis with some intercurrent fever, as typhoid, malarial, etc. 

(2) If the septic symptoms predominate, the case may re¬ 
semble one of typhoid fever, surgical septicaemia, or pyae¬ 
mia. The disease may be mistaken for malarial fever, but 
the chills are too erratic, the temperature does not yield to 
quinine, and the blood-examination does not reveal the 
malarial organism. The disease may also resemble acute 
miliary tuberculosis, but a detailed examination of the case 
and the finding of the bacilli in the sputa will render the 
diagnosis easy. 

(3) If the embolic symptoms predominate, the case may 
resemble non-infective embolism from simple endocarditis, 
acute or chronic, or the secondary suppurative inflammations 
may resemble those of primary origin. Thus the case may 
be mistaken for meningitis, for abscess of the brain, for 
empyema, etc. 

Duration.—Some cases run an acute course of about 
two weeks’ duration. Death results from the derange¬ 
ment of the circulation due to the heart-lesion, from sepsis, 
or from the infective emboli. Other cases run a subacute 


CHRONIC ENDOCARDITIS. 


223 


course of from ten to twelve weeks, and more rarely may 
continue for six or eight months. In these chronic cases 
the infection is less severe, the damage to the heart is less 
extensive, and there is usually an attempt at compensation. 
A few of these chronic cases recover, especially if compen¬ 
sation be perfected and if embolism does not occur. 

The prognosis is generally bad. Only a few cases re¬ 
cover. These cases are those which occur most frequently 
after puerperal infection and which have run a chronic 
course without embolism. These cases, however, are left 
with permanently disabled valves. 

Treatment.—The treatment is that of both the heart in¬ 
flammation and the septic condition. For the heart con¬ 
dition the treatment is that of ordinary endocarditis, but 
carried out more vigorously, and heart stimulants are more 
commonly indicated. 

There are two ways by which the septic condition may 
be treated. One method is by the administration of quinine 
in large doses, so that the patient is kept thoroughly cin- 
chonized. The unpleasant effects of quinine being mitigated 
by adequate doses of phenacetine or sodium bromide, from 
20 to 40 grains of the drug may be given daily. The 
second method consists in the giving of alcohol in large 
doses, so that the patient is kept continuously under its 
influence. 

The secondary suppurations are to be treated on general 
surgical principles. 

CHRONIC ENDOCARDITIS; VALVULAR DISEASE. 

The terms “ chronic endocarditis ” and “valvular disease ” 
are practically synonymous, as it is the endocardium of the 
valves that is almost regularly affected. It is well to dis¬ 
tinguish between two sets of cases, (1) chronic endocarditis 
proper and (2) atheroma. 


224 MANUAL OF THE PRACTICE OF MEDICINE. 


Chronic Endocarditis. 

Pathology.—The lesion consists in the thickening of the 
valve by increased cell-growth and the formation of firm 
connective tissue. In this way the valve-segments become 
contracted, deformed, and insufficient, producing either 
stenosis or insufficiency, or both. Lime-salts may be 
deposited in the thickened valve, so that it may become a 
dense calcareous mass with hardly a vestige of normal 
tissue. There may appear vegetations and ridges formed 
by irregular growth of cells and connective tissue, and upon 
these ridges fibrin may be deposited. Detachment of the 
fibrin in masses will give rise to emboli which are simple and 
non-infective in this disease. The proliferated cells in the 
valve may be the seat of fatty degeneration, producing opaque 
yellow spots frequently infiltrated with salts of lime, or the 
fatty cells may break down, so that little superficial ulcers 
result. To the combination of chronic connective-tissue 
proliferation and fatty degeneration of the cells the name 
“atheroma” is applied. 

Etiology.—Chronic endocarditis regularly follows an 
attack of acute endocarditis produced by any of its causes. 
In some cases, however, it is difficult to obtain a clear 
clinical history of the primary attack. About half the 
cases have a rheumatic origin. The disease is most fre¬ 
quent in children and young adults, and affects the mitral 
valve with the greatest frequency. 

Symptoms.—(i) There are symptoms due directly to the 
diseased valves—aortic stenosis or regurgitation, or mitral 
stenosis or regurgitation. Involvement of the valves of the 
right heart is exceedingly rare. (2) There is developed 
compensatory hypertrophy ; or (3) a dilatation with various 
venous congestions due to the enfeebled pumping power of 
the heart. (4) There may be symptoms of embolism. 


CHRONIC ENDOCARDITIS. 


225 


Atheroma. 

In this class of cases the endocarditis is chronic from the 
start. 

Pathology.—The lesion in the valves is the same as that 
of chronic endocarditis, but is only part of a general set of 
lesions. There is atheroma of the aorta, which may be 
dilated. The small arteries show the lesions of chronic 
endarteritis; their walls are thickened by connective 
tissue and may be infiltrated with lime-salts; their lumen is 
narrowed. In the small arteries of the brain miliary 
aneurysms may be formed. There may be spasm of the 
peripheral arteries. The lungs are frequently emphysema¬ 
tous. The kidneys usually show the lesions of the atrophic 
form of chronic diffuse nephritis. There is frequently 
cirrhosis of the liver. These changes are spoken of under 
the general name “ arterio-capillary fibrosis,” and will be 
described with more detail in a later heading. The aortic 
valves are the favorite seat of the lesion. The mitral valve 
may also be involved, but it is rarely involved alone. 

Etiology.—Atheroma is a disease of adult life, few cases 
being seen before the fiftieth year. It is more common in 
men than in women, and is especially frequent in those 
who lead a life of exposure, intemperance, and severe 
muscular strain. It is thus common in longshoremen. 
Alcoholism, syphilis, gout, chronic rheumatism, and 
chronic lead-poisoning are cited as causes, and there seems 
to be a distinct family predisposition toward this series of 
degenerative changes. 

The symptoms are in the main those of the first class, 
but they differ in the following respects : 

1. The lesion is not only of the heart, but of other 
organs as well, more work being thrown on the diseased 
heart by reason of the increased peripheral resistance in the 

15 


226 MANUAL OF THE PRACTICE OF MEDICINE. 

aorta and the peripheral arteries, and the arterial spasm due 
to the kidney disease. 

2. The lesions occur in late adult life, when recuperative 
powers are on the wane and when compensatory hyper¬ 
trophy is imperfect at the best. 

3. The patients are usually persons leading an intem¬ 
perate life with severe muscular strain, and unwilling— 
indeed, unable—to take the proper care of themselves; by 
reason of their condition of life they are poor subjects for 
compensatory processes. 

4. The lesion is progressive. The valves are not only 
deformed, as in the first class, but tend to become more and 
more involved. 

Detailed symptoms of both sets of cases will be given 
under the head of the individual valvular lesions. 

Mitral Incompetency. 

Etiology.—Insufficiency of the mitral valve results from 
one of three causes: (1) Contraction or shortening of the 
valve-segments from chronic endocarditis, frequently asso¬ 
ciated with changes in the chordae tendineae and with more 
or less narrowing of the orifice. (2) Dilatation of the mitral 
ring from dilatation of the left ventricle. (3) Defective mus¬ 
cular closure from myocarditis, or from the weakening of 
the heart muscle in anaemia and prolonged fever. 

It is important to remember that mitral insufficiency is 
not always a sign of chronic endocarditis, but that the valve- 
segments may be normal, the incompetency being “ relative.” 

Pathology.—As the result of the regurgitation past the 
mitral valve, at each systole of the ventricle the left auricle 
receives blood from two sources—its regular supply from 
the pulmonary veins, and the abnormal supply from the left 
ventricle. The auricle therefore becomes dilated and to 
some extent hypertrophied, although the latter process is 


CHRONIC ENDOCARDITIS. 


227 


never well marked in the case of an auricle. At the time 
of the diastole of the left ventricle this abnormal amount of 
blood at high pressure pours into it, over-filling it. To ac¬ 
commodate this increased amount of blood the ventricle 
must necessarily dilate. Although at the time of the ven¬ 
tricular systole only part of the blood is pumped forward 
in the direction of the normal blood-current, the remainder 
being forced back into the auricle, still, to get rid of the 
large supply of blood, the work of the left ventricle becomes 
excessive, and therefore the ventricle becomes hypertrophied. 
Owing to the over-filling of the auricle during diastole, the 
pulmonary veins are less readily emptied; the right ventri¬ 
cle expels its contents less readily, and becomes both dilated 
and hypertrophied. If the hypertrophy of the right ven¬ 
tricle is adequate to maintain the equilibrium of the pul¬ 
monary circulation, there are no signs of venous congestions 
in the systemic circulation. If compensatory hypertrophy 
fails, however, then general venous congestions will ensue. 

Congestion of the pulmonary vessels is not, as a rule, as 
marked in mitral regurgitation as in mitral stenosis, because 
the back pressure is more intermittent, occurring only dur¬ 
ing diastole, whereas in mitral stenosis it is continuous. 

Cases of relative incompetence due to impaired nutrition 
of the cardiac wall or to its dilatation are not usually well 
compensated. There is apt to be considerable engorgement 
of the pulmonary vessels, with bronchitis and often with 
fairly profuse haemoptysis, and, from general failure in the 
power of the right ventricle to work in face of the pulmon¬ 
ary back pressure, general venous congestions will ensue. 

Symptoms.—If compensation is good, there may be no 
symptoms noticed by the patient even for years. There 
may, however, be some palpitation and dyspnoea on exer¬ 
tion, with a bluish tinge to the lips and the ears. Attacks 
of bronchitis or of haemoptysis may occur. 


228 MANUAL OF THE PRACTICE OF MEDICINE. 


If compensation fails , the symptoms of pulmonary en¬ 
gorgement become more marked; there are palpitation, 
weak and irregular action of the heart, steady dyspnoea with 
developing orthopnoea, increase of cough with bloody or 
watery expectoration, and dropsy, first in the feet and then 
becoming more generally distributed. 

By judicious treatment compensation may again be estab¬ 
lished, and the patient will recover from the attack. Subse¬ 
quent attacks grow more frequent and severe, and recovery 
from them becomes less and less satisfactory, until at last 
a permanent condition of general dropsy and venous con¬ 
gestions results, terminating the life of the patient. Sudden 
death is exceedingly rare. 

Physical Signs.—The characteristic murmur of mitral 
regurgitation is systolic in rhythm, is heard with maximum 
intensity at the apex, and is convected into the left axilla 

and the back. The murmur, 
which may be loud enough to 
be heard over the whole of 
the chest, is usually of a blow- 
ing, puffing character, but it 
may have a musical quality. 
The character of the mur¬ 
mur gives no indication of the 
degree of the insufficiency. 
The murmur may come and 
go, and when absent it may 
frequently be reproduced by 
the upright position, by deep 

the area of cardiac dulness, the point of ^Spirations, Or by exertlOll. 

maximum intensity of the systolic murmur, There are Cases in which the 
and the direction in which it is carried. . 

murmur has its maximum in¬ 
tensity along the left border of the sternum, at the level of 
the second or third rib, where the dilated auricle approaches 






CHRONIC ENDOCARDITIS. 


229 


the chest-wall. There may also be heard the rumbling or 
purring presystolic murmur of an associated mitral stenosis. 
I11 some cases the presystolic murmur alone is heard, even if 
there be regurgitation as well. A systolic thrill is often 
appreciable at the apex, but this sign is not of much diag¬ 
nostic value. 

The second pulmonary sound is accentuated in almost 
all the cases where there is compensatory hypertrophy of 
the right ventricle. This sound is best heard in the second 
interspace to the left of the sternum. 

There are present the ordinary physical signs of hyper¬ 
trophy of the left ventricle, and usually of the right ventricle 
as well, or, in case of failing compensation, the signs of their 
dilatation. 

The pulse may show nothing abnormal, or it may be 
irregular. There is no characteristic sphygmographic 
tracing. 

The diagnosis should be made, not from the presence of 
the murmur alone, but from the other signs as well—the 
accentuated pulmonary second sound, the enlargement of 
the heart, and the clinical history. Mitral incompetency 
should be distinguished in this manner from those haemic 
murmurs which are heard at the apex of the heart, and from 
the so-called “ lung heart ” or the Potain-Rosenbach mur¬ 
mur. This murmur is generated in the overlying lingula 
of lung by the pressure of the heart’s impulse against a 
small bronchus. By this compression at each systole during 
inspiration a systolic puffing sound is produced. This 
sound, however, is not transmitted to the left, and is heard 
only during inspiration. 

The diagnosis of relative incompetence due to anaemia or 
to exhausting disease should be made by a careful review 
of the case. The diagnosis is necessary not only in point 
of prognosis, but also in governing the treatment. 


230 MANUAL OF THE PRACTICE OF MEDICINE. 

Prognosis.—Mitral incompetency is perhaps the least 
serious of all the valvular affections, as it usually occurs in 
young subjects, in whom compensatory hypertrophy is possi¬ 
ble. The prognosis of relative incompetence due to anaemia 
or to exhausting disease is good if the primary disease can 
be cured. The cases which develop in consequence of dila¬ 
tation of the left ventricle usually do badly, as the dilatation 
generally precludes all idea of compensation. 

Mitral Stenosis. 

Etiology.—Mitral stenosis, except for rare congenital 
cases, is always the result of valvular change. The affection 
regularly follows a previous attack of endocarditis, is usually 
seen in early life, and is more common in women than in 
men, in the proportion of 4 to 1, because girls are more 
liable than boys to rheumatism and chorea. The onset of 
the disease is often so insidious that its origin cannot always 
be determined. 

Pathology.—The valve-segments may be stiffened into 
a rigid mass, or they may be fused together, forming a 
conical opening, the “ funnel-shaped mitral.” The orifice of 
the valve may be constricted to form a narrow slit, the “but¬ 
tonhole mitral,” or it may be so constricted as to admit only 
the very tip of the little finger. 

A stenotic mitral valve is almost always incompetent at 
the same time. The effect of the stenosis is to impede free 
passage of blood from the left auricle into the ventricle, 
causing thus steady back pressure, from which other 
changes in the heart result. 

The left auricle becomes much dilated and hypertro¬ 
phied, its muscular walls being increased from two to four 
times in thickness. The over-filled auricle impedes the 
outflow of blood from the pulmonary veins; pulmonary 
engorgement results, being more marked in this than in 


CHRONIC ENDOCARDITIS. 


231 


any other valvular affection. The majority of cases of pig¬ 
ment induration of the lungs are due to this condition of 
engorgement. Dilatation and compensatory hypertrophy 
of the right ventricle result, compensating for the increased 
tension in the pulmonary vessels and equalizing the lesser cir¬ 
culation. In course of time, when the right ventricle fails 
in maintaining its power and hypertrophy, it will weaken 
and dilate, relative incompetence of the tricuspid valve will 
ensue, and general venous congestions will presage a fatal 
issue. 

In uncomplicated mitral stenosis less than the normal 
amount of blood enters the ventricle to be pumped into the 
arteries; hence less work is required of the ventricle, and 
neither dilatation nor hypertrophy should occur. In cases, 
however, associated with incompetency of the valve, hyper¬ 
trophy or dilatation of the ventricle occurs. In rare cases 
the ventricle may hypertrophy without any appreciable 
cause. It is supposed that increased peripheral resistance 
from general contraction of the arteries, caused by their 
irritation by imperfectly-oxidized blood owing to pulmo¬ 
nary congestion and engorgement, might account for these 
cases. 

The symptoms of mitral stenosis resemble those of 
mitral regurgitation, both conditions producing the same 
results—arterial anaemia and venous congestions, first in the 
pulmonary system, later in the systemic veins when failure 
of the right ventricle occurs. Symptoms of pulmonary 
congestion are, however, more marked and constant in 
stenosis than in insufficiency. Children with mitral stenosis 
are usually poorly developed. 

Physical Signs. —The cardiac impulse is often most 
appreciable in the region of the lower sternum and in the 
fourth and fifth left interspaces, being caused by the hyper¬ 
trophied and dilated right ventricle approaching the chest- 


232 MANUAL OF THE PRACTICE OF MEDICINE. 


wall in these situations. Localized just above and within 
the apex may be felt a distinct vibratory or “ cat’s-purr ” 
thrill. This thrill is presystolic and terminates with a 
sudden sharp shock synchronous with the cardiac impulse. 
When present, it is pathognomonic of mitral stenosis. Care 
should be taken not to mistake this apex thrill for a 
diastolic thrill at the base due to aortic regurgitation. 


The murmur of mitral stenosis is heard to the inner side 

of the apex beat over a limited 
area (Fig. 12), and is not trans¬ 
mitted in any direction. Its 
rhythm is presystolic, or, more 
properly speaking, auricular- 
systolic ■, as the murmur is pre¬ 
systolic only as regards the 
ventricular systole. The mur¬ 
mur is a rough, rolling, purr¬ 
ing sound, represented by 
pronouncing “ rup ” or “ r-r-r- 
rup,” having in the latter case 
a rolling drum-beat character. 
It may terminate abruptly with 
the first sound, which is un¬ 
usually clear and snappy, or 
there may be a distinct interval 
between the sounds. The murmur may consume a good 
part of the diastole, or it may be heard only during the latter 
part of it. The murmur often comes and goes, usually dis¬ 
appearing if compensation fail, only to reappear should 
compensation again be established. It is often heard better 
with the ear than with the stethoscope. 

If regurgitation coexist with stenosis, there will also be 
heard the murmur of the former affection ; this murmur may 
be so faint as to be heard only when the breath is held. 



Fig. 12.—Mitral stenosis, showing area 
of cardiac dulness, location of the presys¬ 
tolic murmur, and the area over which 
it is heard. 




CHRONIC ENDOCARDITIS. 


233 


Valuable evidence is afforded by the second pulmonary 
sound. This sound, which is sharply accentuated if the 
right ventricle is doing its work well, is reduplicated in 
about one-third of all cases, and its reduplication is strong 
presumptive proof of mitral stenosis. The second aortic 
sound is weak, as the amount of blood entering the aorta 
is insufficient to raise its tension. 

Hypertrophy and dilatation of the left auricle and the 
right heart, and possibly of the left ventricle as well, give 
their customary physical signs. 

The pulse of mitral stenosis is small as compared with the 
action of the heart, the arteries being under-filled. 

A characteristic of mitral stenosis is the occurrence of 
interpolated beats in the line of the descent of the pulse- 
wave. These interpolated beats, which are well seen in the 
accompanying sphygmographic tracings (Figs. 13, 14), are 



Fig. 13.—Sphygmogram showing the interpolated beats of mitral stenosis. 



Fig. 14.—Sphygmogram showing the interpolated beats of mitral stenosis. 

little abortive systoles, started as extra contractions of the 
overloaded auricles and communicated thence to the ventri¬ 
cles. As their irregular systoles occur during the time of 







































234 MANUAL OF THE PRACTICE OF MEDICINE. 

diastole, when the ventricle is under-filled with blood, a dis¬ 
tinct and well-marked pulse-wave cannot be formed. 

Diagnosis. —The murmur of mitral stenosis may be mis¬ 
taken for the diastolic murmur of aortic regurgitation, trans¬ 
mitted down to the apex and heard there late in the diastole. 
Examination at the base of the heart should reveal the max¬ 
imum intensity of the aortic murmur. The character of the 
pulse should assist in the differential diagnosis. The diag¬ 
nosis is more difficult if the murmur be absent. The diag¬ 
nosis must be made upon the accentuated or reduplicated 
second pulmonary sound, the weak second aortic sound, the 
sudden, snappy first sound at the apex, and the physical 
signs of enlargement of the right ventricle. 

The prognosis in mitral stenosis is not so good as that 
in mitral insufficiency, because the back pressure of the 
pulmonary veins is constant and not intermittent, and be¬ 
cause the force of the left ventricle cannot be called into 
requisition to aid in the compensation of the lesion. 

Aortic Regurgitation. 

Etiology. —Insufficiency of the aortic valves may be 
caused by the following conditions: 

1. Congenital lack of development. 

2. Rupture of a valve-segment. A healthy valve-flap 
may in rare instances be caused by excessive strain, such as 
heavy lifting; or an ordinary strain maybe the means of 
rupturing a valve that is weakened by ulcerative changes. 

3. Stretching of the aortic ring , causing “ relative incom¬ 
petence.” This condition is rare, and is seen only in cases 
of extensive atheroma of the aorta with great dilatation just 
above the valves. 

4. Acute endocarditis. Aortic incompetence does not re¬ 
sult during an acute attack unless the valve be eroded or 
ulcerated. It is more commonly seen, therefore, in malig- 


CHRONIC ENDOCARDITIS. 


235 


nant endocarditis. Slow changes, however, may result in 
the shrinkage, contraction, and calcification of the valve, 
causing it to become incompetent. Aortic incompetency 
may thus be seen in children with antecedent history of 
rheumatism and acute endocarditis, but it is not so common 
under these circumstances as mitral disease. 

5. By far the most common cause of incompetence is the 
slow contraction due to atheroma, seen in able-bodied 
laborers who are subject to heavy muscular labors and who 
over-indulge in alcohol. There may be a syphilitic 
element which of itself is capable of causing arterial 
sclerosis. Occurring as the result of atheroma there are 
apt to be found associated lesions in the aorta, arteries, 
kidneys, liver, and lungs, already alluded to (see Atheroma, 
page 225). 

Pathology.—As the result of the incompetency of the 
aortic valve, blood flows from the aorta back into the 
ventricle during the diastole. The left ventricle then 
receives blood from two sources—the normal supply from 
the auricle, and the regurgitated blood from the aorta. 
The ventricle therefore becomes greatly dilated. Dilatation 
is all the more extreme because the distention of the 
ventricle occurs during diastole, at which time the tissues 
are in a relaxed condition, and also because the heart-wall 
is often the seat of fatty degeneration, as will be shown 
hereafter. The increased labor of expelling this large 
amount of blood, part of which is to roll back again, leads 
to hypertrophy of the left ventricle. This hypertrophy 
reaches the highest degree seen in any valvular disease, 
and may produce a heart of enormous size and weight (from 
30 to 50 ounces), to which the name “ bovine heart,” or cor 
bovinum , has been applied. This is especially the case in 
children. 

Relative incompetence of the mitral valve is common as 


236 MANUAL OF THE PRACTICE OF MEDICINE. 

the result of the dilatation of the left ventricle; when this 
incompetence occurs there is apt to be pulmonary conges¬ 
tion with compensatory hypertrophy of the right ventricle. 

There is a tendency in aortic regurgitation for the heart 
to undergo fatty or fibroid degeneration from poor coronary 
circulation, either because of the associated atheroma or 
calcification of the coronary arteries, diminishing their cali¬ 
bre, or because the coronary arteries, by reason of the dimin¬ 
ished tension in the aorta, are poorly filled with blood. 

Aortic regurgitation is often associated with aortic 
stenosis, but regurgitation alone is more common than 
stenosis alone. Aortic aneurysm may complicate the 
valvular disease. In advanced cases there may be changes 
in the cardiac nerves and ganglia that may lead to angina 
pectoris. 

Symptoms. —As long as the hypertrophy equalizes the 
valvular defect there are no characteristic symptoms. In 
advanced cases with myocardial degeneration or with 
lesions in the aorta and coronary vessels there are apt to be 
developed symptoms of arterial ancemia —headache, dizzi¬ 
ness, irritability of temper, faintness even to the point of 
syncope, palpitation, dyspnoea on exertion, with the general 
symptoms of anaemia. There may be dull aching pain in 
the precordium, or else attacks of angina pectoris. If at any 
time the diastole be unduly prolonged, the regurgitating 
blood may so empty the aorta and large vessels as to cause 
sudden cerebral anaemia. Sudden death may occur under 
these circumstances, and its possibility must always be 
considered in making the prognosis. CEdema of the feet 
and dyspnoea with progressing symptoms of venous con¬ 
gestion usher in a fatal issue, and differ in no essential 
features from the venous congestions and heart failure of 
other valvular lesions. 

The physical signs of aortic regurgitation are apt to be 


CHRONIC ENDOCARDITIS. 


237 


clean-cut and distinctive. The characteristic murmur, which 
is diastolic in rhythm, replacing the second sound, is 
usually heard best in the mid-sternum, at the level of the 
third rib, and is convected downward toward the lower end 
of the sternum and the apex. It may be heard best in the 
second right interspace or at the lower end of the sternum, 
or even just within the apex. If heard in these latter 
localities, to which it has been convected downward, it may 
closely resemble the presystolic murmur of mitral stenosis. 
Aid to diagnosis in such cases is afforded by the presence 
of the murmur at the base of the heart as well, and by the 
other physical signs. Often the murmur is better heard 
with the ear than with the stethoscope. It may be harsh 
and of a “ sawing ” character, or it may be a soft, long-drawn 
bruit. It is very constant and reliable. 

The first sound at the apex is usually weak, and may be 
replaced by the murmur of relative incompetence of the 
mitral valve. 

The first sound at the base may be replaced by a mur¬ 
mur. This may mean stenosis of the aortic valve, or merely 
roughening of the surface of the valve or of the intima of 
the aorta just above the valve. 

There may be a distinct diastolic thrill over the base of 
the heart. This thrill may be so diffused as to reach the 
apex and be then mistaken for the thrill of mitral stenosis; 
but it is not limited to the apex, nor does it terminate with 
the sharp shock of the cardiac impulse, as does the thrill of 
mitral stenosis. 

The character of the pulse gives material aid in diagnosis. 
There is visible pulsation of the peripheral arteries, even in 
the vessels in which pulsation is not normally visible. The 
arteries may appear tortuous, straightening themselves with 
a peculiar jerky motion with each systole. There may be 
capillary pulsation under the finger-nails or over any skin 


238 MANUAL OF THE PRACTICE OF MEDICINE. 

area artificially reddened by friction. However common 
this sign may be in aortic regurgitation, it is also seen in 
profound anaemia, in neurasthenia, and in conditions asso¬ 
ciated with great relaxation of the peripheral arteries, and 
hence is not in any sense pathognomonic. 

There may be pulsation in the second right intercostal 
space or in the suprasternal notch that may lead to the 
diagnosis of aneurysm. There may be a diastolic pulsation 
of the liver, even if the tricuspid valve be competent. Oph¬ 
thalmoscopic examination reveals visible pulsation of the 
retinal arteries of a characteristic jerking quality. 

There is heard a to-and-fro murmur in the femoral artery. 
On palpation the characteristic “ water-hammer ” or “ Cor¬ 
rigan ” pulse is felt. The pulse strikes the finger with a 
sudden forcible impulse, and then at once collapses, leaving 
the artery empty. This is best appreciated at the radial 
artery when the hand is held above the head. The quality 
of the pulse is plainly recognized in the sphygmographic 
tracing (Fig. 15). 



Fig. 15.—Sphygmogram of aortic regurgitation. 


Associated with these characteristic signs of aortic re¬ 
gurgitation are those depending upon the increased size 
and muscular power of the heart. There is a wide forcible 
area of cardiac impulse, the apex beat often being in the 
sixth or seventh interspace, and being perhaps as far dis¬ 
placed as the anterior axillary line. There may be bulging 
of the precordium in children. This increase of size, also 
determined by percussion, is due to dilatation and hyper- 





CHR ONIC END OCA RD1TIS. 


239 


trophy of the left heart, and possibly of the right heart as 
well. 

The prognosis in aortic regurgitation is not good, for 
three reasons: (1) As the 
affection occurs usually in 
elderly overworked alcoholic 
subjects as a degenerative 
change frequently associated 
with arterial and renal lesions, 
compensation is neither com¬ 
plete nor sustained. (2) From 
the frequent complication of 
fatty degeneration of the heart- 
muscle, there is a tendency 
to sudden or gradual heart 
failure. (3) There may at any 
time be a sudden over-dis¬ 
tention of the ventricle, caus¬ 
ing its paralysis, and the sud¬ 
den death of the patient from 
acute cerebral anaemia. The liability to sudden death 
should always be remembered in giving the prognosis. 



Fig. 16.—Aortic regurgitation, showing 
the area of cardiac dulness, the usual points 
of the maximum intensity of the diastolic 
murmur, and the direction in which it is 
carried. 


Aortic Stenosis. 

Etiology. —The lesion of aortic stenosis may be the re¬ 
sult of chronic endocarditis following an acute attack caus¬ 
ing thickening and rigidity of the valve. Usually, however, 
the disease occurs in old people as an atheromatous change, 
and is associated with some degree of incompetency. The 
latter condition is the more serious, and stamps the disease 
with its own characteristics. 

Pathology. —The valve-segments may be simply adherent 
to each other, or they may be thickened, contracted, or cal¬ 
cified. There may be a tongue of fibrin or large vegetations 




240 MANUAL OF THE PRACTICE OF MEDICINE. 

projecting into the orifice, further obstructing it. do over¬ 
come the obstruction to the onward passage of blood through 
the aortic outlet, more force is required of the left ventricle. 
It consequently hypertrophies. Usually there is but little 
dilatation. The whole force of the ventricle being thus 
called into requisition, compensation is usually good and 
the remaining parts of the heart are not affected. It is only 
when the left ventricle begins to fail that there is dilatation 
of the auricle, impeded pulmonary circulation, and increased 
work for the right heart. 

Symptoms.—There are no symptoms characteristic of 
aortic stenosis. The affection may last for years and be dis¬ 
covered finally by accidental examination. In advanced 
cases, where a lessened amount of blood enters the aorta 
with each systole, there may be symptoms of anaemia, such 
as dizziness, faintness, and spots before the eyes. In more 
advanced cases there may be Cheyne-Stokes breathing 
during the latter part of the disease. When compensation 
fails the symptoms of pulmonary and systemic congestion 
do not differ in any way from those caused by other 
valvular affections. 

Physical Signs.—The characteristic murmur is systolic, 
heard best in the second right interspace, and is conducted 
upward along the course of the great vessels. Such a 
murmur is not distinctive of aortic stenosis, as it may be 
caused as well by simple roughening of the aortic valve or 
of the intima of the aorta above the valve, or by anaemia. 
If due to stenosis, the murmur is frequently harsher than 
if due to the other causes, but even then it may become 
faint and distant if the left ventricle begin to fail. The 
second sound at the aortic area is usually weak from 
diminished blood-pressure in the aorta at the time of the 
diastolic closure of the valve. This sign may be of great 
aid in diagnosis. In other cases the second aortic sound is 


CHRONIC ENDOCARDITIS. 


241 


replaced by the murmur of aortic regurgitation. There is 
frequently at the base a systolic thrill which may be very 
well marked. There are the 
ordinary physical signs of 
hypertrophy of the left ven¬ 
tricle, and, in the later stages, 
of its dilatation, and with the 
dilatation the enlargement of 
the right heart from hyper¬ 
trophy or dilatation. The 
pulse is small in size, is regu¬ 
lar in rhythm, and may be 
somewhat slow. 

Prognosis.— In simple ste¬ 
nosis the prognosis is gener¬ 
ally good, as compensation 
is easily accomplished by 
hypertrophy of the left ven¬ 
tricle. If the stenosis be ac¬ 
companied by regurgitation, the prognosis will depend upon 
the latter condition. 



Fig. 17.—Aortic stenosis, showing the 
area of cardiac dulness, the point of maxi¬ 
mum intensity of the systolic murmur (X), 
and the direction in which it is carried. 


Tricuspid Regurgitation. 

This condition may result as an acquired affection in 
endocarditis, especially in the malignant form. 

Relative incompetence is far more common, and is due 
to dilatation of the right ventricle with stretching of 
the tricuspid ring, or to poor muscular contraction of the 
ventricle. It is thus produced by a failing left heart, and 
by any cause producing obstruction in the pulmonary cir¬ 
culation, such as emphysema and interstitial pneumonia. 
In either case it is a consequence of failure in compensation 
of the right ventricle. When tricuspid regurgitation occurs, 
the blood at the time of systole regurgitates from the right 
16 





242 


MANUAL OF THE PRACTICE OF MEDICINE. 


ventricle into the auricle and the veins, with the production 
of venous congestions. 

The physical signs of tricuspid regurgitation are—(1) 
A systolic murmur, usually low and soft, heard with maxi¬ 
mum intensity at the lower part of the sternum, and trans¬ 
mitted to the right, frequently as far as to the axilla. (2) 
Enlargement and fulness of the jugular veins. (3) A 
venous pulsation in the superficial veins of the neck, and 
frequently a pulsation of the liver. This latter sign is best 
made out by bimanual palpation, and should not be con¬ 
founded with the apparent pulsation imparted to the liver 
by an over-acting right ventricle. (4) Marked increase of 
general venous congestions. 

Tricuspid Stenosis. 

Congenital cases of tricuspid stenosis are not uncommon. 
The acquired form occasionally occurs, usually associated 
with lesions of the left heart, especially with mitral stenosis. 

As the only means of compensation is by hypertrophy 
of the relatively weak right auricle, effectual compensation 
cannot occur. Marked venous congestions with great 
cyanosis are the inevitable result. 

The physical signs of tricuspid stenosis are—(1) A pre- 
systolic murmur heard at the base of the ensiform carti¬ 
lage. (2) Hypertrophy and dilatation of the right auricle. 
(3) Occasionally a presystolic thrill over the lower part of 
the sternum. 


Pulmonary Regurgitation. 

This affection, which is almost invariably the result of 
congenital malformation, is exceedingly rare. The regurgi¬ 
tation of blood backward into the right ventricle is followed 
by great dilatation, and relative incompetence of the tri¬ 
cuspid valve is very apt to result. 


CHRONIC ENDOCARDITIS. 


243 


Compensation is necessarily imperfect, and a fatal issue is 
not long delayed. 

The physical signs of pulmonary regurgitation are—(1) 
A diastolic murmur heard in the second left interspace, and 
convected downward and to the right. It is difficult to 
differentiate the murmur from that of aortic regurgitation. 
(2) Enormous hypertrophy and dilatation of the right ven¬ 
tricle. (3) The physical signs of the relative incompetence 
of the tricuspid valve. 

Pulmonary Stenosis. 

This affection, which is of great rarity except as the re¬ 
sult of disease or of arrested development during intra-uterine 
life, is one of the commonest forms of congenital malforma¬ 
tions, and is often associated with an open foramen ovale 
or an imperfect interventricular septum. As an acquired 
disease it may result from malignant endocarditis. 

There is considerable hypertrophy of the right ventricle, 
with dilatation, but compensation is seldom perfect, being 
easily upset by intercurrent pulmonary affections. The dila¬ 
tation of the right ventricle allows of tricuspid regurgitation 
(relative incompetence) in the majority of cases. 

The physical signs of pulmonary stenosis are—(1) A 
systolic murmur heard in the second left interspace, and 
convected a short distance upward and to the left. (2) 
A weak or absent second pulmonary sound. (3) Marked 
hypertrophy and dilatation of the right heart. (4) There 
may be the murmur of relative incompetency of the tri¬ 
cuspid valve, with fulness and possibly pulsation of the 
superficial veins, especially those of the neck. 

Treatment of Chronic Valvular Disease. 

The treatment of chronic valvular disease may be divided 
into that of the stage of compensation and that of its failure. 


244 MANUAL OF THE PRACTICE OE MEDICINE. 

Stage of Compensation.—Hypertrophy is in itself com¬ 
pensatory of valvular defects, and if the circulation be main¬ 
tained by it so that the arteries are kept filled and the 
venous flow is not obstructed, there is no medicinal treatment 
necessary. Much harm is done by injudiciously prescribing 
digitalis whenever a murmur is heard, no regard being paid 
to whether the lesion is compensated or not. Still, it is 
necessary that compensation should be maintained. The 
balance between the available power of the heart and the 
work required of it may be so delicate as to be upset easily 
by weakness on the one side or by increase of work on the 
other. Should the patient run down by reason of old age, 
sickness, or vicious habits, the myocardium will become 
degenerated and its power will be weakened, while, on the 
contrary, the hypertrophy may be inadequate to meet any 
demand for increased work. 

1. The patient should be kept, in good health. To secure 
intelligent co-operation it may be necessary to inform the 
patient of the lesion, although it is usually best to confide 
in some intimate friend or member of the family, upon whose 
judgment reliance can be placed. The patient should 
lead a quiet, orderly, and well-regulated life. The diet 
should be simple and wholesome, and all digestive errors 
are to be corrected by appropriate measures. Tobacco, tea, 
and stimulants should be avoided. Turkish baths should 
be eschewed, and the patient should not live in too high an 
altitude. Mental worry, over-fatigue, and severe bodily 
exposure should be avoided. As the prognosis of valvular 
disease with compensation is much better than was formerly 
supposed, and as sudden death occurs only with aortic re¬ 
gurgitation, the patient, if informed of his complaint, should 
be so encouraged and stimulated as to dispel mental depres¬ 
sion and despondency. 

2. The work thrown o?i the heart should be lessened as 


chronic Endocarditis. 


245 

much as possible. In almost all eases enough exercise 
should be taken to keep the general health good. In fact, 
the heart’s power may even be developed by graduated 
exercise. Oertel recommends ascending hills of increasing 
steepness and length until compensation is fully established. 
At no time, however, should exercise or work ever be 
allowed to pass to the point of excessive fatigue, nor should 
sudden violent exercise be permitted. Mental excitement 
of all kinds should be interdicted. 

The condition of arterial tension should always be deter¬ 
mined. Should it be raised, pointing to increased periph¬ 
eral resistance, it should be reduced and kept reduced. 

The diet should be simple; over-eating and drinking are 
to be checked; the bowels must be kept open and diuretics 
be administered. These procedures may suffice without 
the need of drugs. Should the latter be indicated, iodide 
of potassium (gr. x t. i. d.), chloral hydrate (gr. v to vii t. i. d.), 
and nitroglycerin (gr. ^ q. 3 h.) are of the greatest value. 

Treatment of Failing Compensation.—The treatment 
naturally is to be directed to fulfil four indications : 

1. To lessen the work required of the heart. 

(a) By rest. This of itself may restore disturbed com¬ 
pensation, and should be resorted to in all serious cases. 
The patient should be put to bed and kept quiet, or, in less 
severe cases, confined to the room. 

(b) By avoidance of over-action of the heart by emotional 
excitement, alcohol, tea, coffee, tobacco, or sexual excesses. 

(c) By diminishing peripheral arterial resistance , should 
any exist, by regulating the diet, by increasing elimination 
of offending waste products by the skin, kidneys, and 
bowels, and by the administration of potassium iodide, 
chloral, or nitroglycerin. 

2. To improve the force of the heart. The best drug for 
this purpose is digitalis. Digitalis is contraindicated in 



246 MANUAL OF 7 'HE PRACTICE OF MEDICINE. 

perfectly-balanced compensatory hypertrophy. The indi¬ 
cation for its use is broken compensation, no matter from 
what valvular affection. When digitalis does good the 
pulse becomes fuller, more regular, and of better tension, 
the dyspnoea and oedema diminish, and the urine usually 
increases in quantity. There are cases in which it does 
good even if the pulse continues irregular. Toxic effects 
may, however, be produced by its injudicious administration, 
and are shown by nausea and vomiting. The urine is reduced 
in amount. The pulse becomes irregular, and there may 
be two heart-beats to one of the pulse, especially in mitral 
stenosis. The particular preparation of digitalis to be used 
is of no consequence if the drug be good. Only as large 
doses should be given as may be required; over-stimulation 
should be avoided. Some patients in serious conditions 
may require large doses—from 15 to 20 minims of the 
tincture every three hours—while other cases, less aggra¬ 
vated, do well on from 3 to 4 minims two or three 
times a day. As a certain increase in the rapidity of the 
heart is one of the methods of compensation for a valvular 
lesion, digitalis should not be given blindly to reduce the 
frequency of the pulse to normal. The proper administra¬ 
tion of digitalis requires the greatest judgment and the 
detailed watching of the patient. 

In aortic regurgitation digitalis may do harm by unduly 
prolonging the diastole, so giving time for the ventricle to 
become over-distended. In such cases opium in gr. j doses 
three times a day is often of service. 

Strophanthus in the form of the tincture (gr. v to viii) 
may be employed instead of digitalis. It is often of 
service in steadying an intermittently acting heart, but it is 
inferior to digitalis in power. 

Convallaria, caffeine, and adonis vernalis are not now so 
extensively used as formerly. They may be given, how- 


CHRONIC ENDOCARDITIS. 247 

ever, should digitalis disagree with the stomach. Iron and 
strychnine are often of great value. 

The timely administration of iron, with or without arsenic, 
often restores tone to the system and checks failing compen¬ 
sation. Strychnine is of great service, combined with digi¬ 
talis, in increasing the force of the heart. When the pulse 
is intermittent and irregular, iodide of potassium may be 
given, either alone or with digitalis. It is often of the 
utmost service. Nitroglycerin is a valuable heart tonic to 
meet temporary indications. It may be combined with 
digitalis. 

When the heart’s action is rapid and tumultuous, much 
good is done by cold applications over the heart. When 
the heart-action is weak and irregular, constant irritation 
over the heart by a nitric-acid issue is of great service. 

3. To diminish the venous congestions. 

(a) By venesection. In cases of dilatation from whatever 
cause, with venous congestions, cyanosis, and dyspnoea, 
much relief is experienced by the withdrawal of from 15 to 
25 ounces of blood. Timely venesection may save the pa¬ 
tient’s life in acute cases. 

(li) By purgation. This is of service especially in cases 
with dropsy. From l / 2 ounce to \]/ 2 ounces of Epsom salt 
may be given in a concentrated form half an hour before 
breakfast. The compound jalap powder, or elaterium, or any 
other hydrogogue cathartic may be given, and is usually 
well borne. 

(c) By diuresis. For this purpose digitalis, with or with¬ 
out a saline diuretic, potassium citrate or acetate, is most 
efficient. In almost every case a sure indication that digi¬ 
talis is doing good is the increase in the quantity of the 
urine. 

Calomel in gr. iij doses every six hours for three or four 
days is often of the greatest service in cardiac dropsy, acting 


248 MANUAL OF THE PRACTICE OF MEDICINE. 

both as a diuretic and a cathartic. It should be discontinued 
should stomatitis develop. 

A favorite combination is the pill composed of a grain 
each of powdered digitalis, squills, and blue mass. Iodide 
of potassium in gr. x doses is often an efficient diuretic. If 
the blood-tension be abnormally high, diuresis may be in¬ 
creased by the reduction of the tension by iodide of potas¬ 
sium, nitroglycerin, or chloral hydrate. When the urine 
is greatly diminished, cups and poultices over the kidneys 
often prove of the utmost value. 

( d ) By operative interference. Serous accumulations in 
the pleural or peritoneal cavities may interfere to such an 
extent with the respiration and the heart’s action that aspira¬ 
tion under the strictest antiseptic precautions may be re¬ 
sorted to. Frequently, after tapping ascitic fluid, diuretics 
and cathartics, formerly of no avail, will succeed in prevent¬ 
ing reaccumulation. 

If the oedema of the legs be unrelieved by depletion 
through the bowels and kidneys or by elevation and band- 
aging of the feet and legs, scarification of the skin may be 
resorted to, or Southey’s tubes—small silver cannulae with 
tubing attached—may be inserted under the skin ; but these 
methods are recommended only in the very severest cases. 

4. To improve the general condition. While the symptoms 
incident to the deranged circulation are being treated, every 
attempt should be made to support the general health of 
the patient and to control all symptoms that interfere with 
sleep or with general nutrition. The diet should be simple, 
nutritious, and easily digestible. Over-distention of the 
stomach by food or by gas should be avoided. Iron and 
general tonics should be given. It is important that the 
patient should enjoy a restful sleep at night. For this pur¬ 
pose sulphonal, chloralamide, or trianol may be given. In 
milder cases Hoffmann’s anodyne, camphor-water, valerian, 


Acute myocarditis . 


249 


or bromide of sodium may suffice. In aggravated cases 
of insomnia with dyspnoea and restlessness nothing acts 
more pleasantly than morphine, preferably given hypoder¬ 
mically. Opium by the mouth may be given to these 
patients in divided doses throughout the day. 


3. DISEASES OF THE MYOCARDIUM. 

ACUTE MYOCARDITIS. 

This disease occurs in two forms: 

1. Acute Diffuse Myocarditis. —This disease occurs in the 
course of infectious diseases and in septic processes of all 
kinds, and seems to be due to poisoning of the heart-muscle 
by bacterial products. It is best seen in fatal cases of diph¬ 
theria. It may complicate endocarditis or pericarditis. 
The heart-muscle is soft; its color is dark red with hemor¬ 
rhagic points, or it may be yellowish-red or mottled. The 
heart-cavities are frequently dilated. The muscle-fibres un¬ 
dergo granular degeneration and may become fatty. The 
interstitial fibrous structure is infiltrated with round cells. 
The left ventricle is more frequently involved than the right. 
The disease may terminate in complete recovery or in 
chronic fibroid myocarditis, or it may end in suppuration. 

2. Acute Circumscribed Myocarditis , or Acute Suppurative 
Myocarditis. —This form of myocarditis is due to infection 
of the heart-muscle by suppurative micro-organisms which 
arise from a primary focus of suppuration and reach the 
heart as emboli. Examination reveals small scattered foci 
of suppuration in the heart, in the form of grayish or of yel¬ 
low spots or streaks, usually surrounded by a hemor¬ 
rhagic zone. They are most common in the anterior wall 



250 MANUAL OF THE PRACTICE OF MEDICINE. 

of the left ventricle and in the septum, but they may occur 
in any locality. A suppurative focus may rupture into the 
pericardium, producing suppurative pericarditis, or into the 
heart-cavities, producing malignant endocarditis, general 
septicaemia, or suppurative emboli. These complications 
may occur without apparent rupture. Aneurysm of the 
heart and rupture of its wall may occur. The disease is 
almost always fatal, as the result of the cardiac condition or 
of the primary disease. Rarely the abscesses become en¬ 
capsulated, the pus becomes inspissated, or a calcareous 
nodule may remain. 

Symptoms.—The symptoms of both forms of myocar¬ 
ditis are indefinite and are obscured by those of the 
primary disease. There is, however, a sudden increase of 
cardiac weakness; the pulse becomes rapid, irregular, and 
feeble; dyspnoea becomes marked. The heart-cavities 
usually dilate, and may occasion grave disturbances of cir¬ 
culation. Sudden death may occur, even in patients who 
have not been considered seriously ill. This termination is 
especially seen in diphtheria. 

The physical signs are those of weakened action of the 
heart, and possibly some increase in its size by dilatation. 
There may be the murmur of mitral regurgitation from 
relative insufficiency. The sounds are weak and may be 
equidistant, giving “ tick-tack ” sounds resembling those 
of the fetal heart. The occurrence of such “ embryocardia ” 
is always of serious import. 

The prognosis is always grave except in the lighter 
degrees of the diffuse form. 

Treatment.—The patient should be kept in absolute rest. 
Cold applications to the precordium seem to be of service, 
and alcohol should be administered freely. Digitalis does 
not seem to be of much service; if given in large doses it 
may be the means of rupturing a heart abscess. 


CHRONIC MYOCARDITIS. 




CHRONIC MYOCARDITIS. 

Etiology and Synonyms.—This disease may follow acute 
diffuse myocarditis or areas of anaemic necrosis. It is seen 
in chronic poisoning by alcohol, syphilis, or gout. It may be 
associated with pericarditis or endocarditis, Its most com¬ 
mon cause, however, is the narrowing of the coronary arteries, 
producing either low-grade tissue-changes from defective 
blood-supply, or thrombus-formation resulting in infarctions 
which gradually become converted to fibroid areas. The 
affection is thus commonly met with in people of ad¬ 
vanced age who have indulged freely in alcohol and 
high living, who have had syphilis, and who have done 
hard work. In such patients renal disease, endarteritis, 
and fibroid myocarditis are usually associated. Synonyms: 
Fibroid heart; Fibroid myocarditis; Chronic interstitial 
myocarditis. 

Pathology.—The lesion may be diffuse or circumscribed. 
The parts most frequently affected are the wall of the left 
ventricle, the papillary muscles, and the septum. The 
affected areas are firm, cut with resistance, and are opaque 
and grayish in appearance. The lesion consists in the 
increase of connective tissue with atrophy or degeneration 
of the muscle-fibres. The coronary arteries generally show 
obliterating endarteritis. The heart is usually enlarged 
and hypertrophied. Localized fibroid areas may allow of 
sacculated dilatation of the heart. 

Symptoms.—In some cases of chronic myocarditis there 
are no symptoms, the lesion being accidentally found post¬ 
mortem. In other cases there may be sudden death, which 
may occur without previous symptoms of disease. In still 
other cases there are symptoms of weakened power of the 
heart with circulatory disturbances. Palpitation and dysp¬ 
noea are common. There may be attacks of angina 


252 MANUAL OF THE PRACTICE CE MEDICINE. 

pectoris, which may be the only symptom. Intermis¬ 
sions and inequalities of the pulse are common, and the 
pulse is usually slow, being frequently reduced to 40 or 50 
beats in the minute. There may be sudden syncope, 
coming usually after exertion, in which attack the patient 
may die. Attacks of coma resembling cerebral hemorrhage 
may occur and may prove fatal. There may finally be any 
of the symptoms of a dilated heart with venous congestions. 

The physical signs are uncertain. The heart is usually 
enlarged in size ; its sounds are weak. 

Diagnosis. —Aid is afforded by the presence of the 
arterial degenerative changes of nephritis and by the 
occurrence of symptoms of a failing heart without the signs 
of actual dilatation or valvular lesion. T he diagnosis from 
fatty degeneration is almost impossible. 

Prognosis. —The patient may live for years, but death 
may occur at any time from an attack of angina, of syn¬ 
cope, of coma, or without antecedent symptoms. 

Treatment. —In general terms, the treatment is that of 
fatty degeneration. Iodide of potassium is indicated in 
syphilitic cases. Heart stimulants are demanded by signs 
of cardiac weakness. Alcohol, strychnine, and nitro¬ 
glycerin are to be employed for this purpose, as digitalis is 
contraindicated because of the already increased blood- 
pressure in the sclerotic arteries. The diet should be 
simple; the habits of life are to be well regulated, and 
exercise is to be taken regularly and sparingly, and never 
suddenly nor to excess. 

SYPHILITIC MYOCARDITIS. 

Two forms of syphilitic myocarditis are recognized: 

1. A Diffuse Fibroid Myocarditis .—This variety cannot be 
distinguished from the ordinary form by either physical 
signs or clinical symptoms. 


degeneration of THE MYOCARDIUM. 253 

2. Gumnicita in the Myocardium .—These gummatous 
tumors weaken the heart-muscle, causing symptoms of 
heart weakness, and may result in sudden death or in 
ruptuie of the heart. A positive diagnosis can be made 
only in cases where marked improvement follows the 
administration of large doses of potassium iodide in syphi¬ 
litic subjects with heart weakness. 

DEGENERATION OF THE MYOCARDIUM. 

1. Anaemic Necrosis, or white infarct, a localized degen¬ 
eration of the myocardium, occurs as the result of the 
occlusion of a coronary artery or of one of its branches by 
thrombosis or embolism. Thrombosis is favored by 
sclerosis and atheroma of the wall of the vessel. The 
anterior coionary artery is usually the one involved, so that 
the resulting anaemia-necrosis is found in the left ventricle 
or in the septum. The patch is anaemic, whitish or grayish 
in color, and is usually of an irregular w T edge shape. It 
may soften and break down, and may even result in rupture 
of the heart, or it may undergo hyaline degeneration and 
ultimately become sclerotic, forming the lesion of fibroid 
myocarditis. Such a blocking of the coronary artery is 
one of the common causes of sudden death, and the lesion 
should always be looked for in these medico-legal cases. 
In other cases there are angina pains with feebleness of the 
heart’s action. There may be a series of such attacks, any 
one of which may prove fatal. 

2. Parenchymatous degeneration, or “cloudy swelling,” 
is seen in the course of infectious diseases, especially diph¬ 
theria, typhoid, and scarlet fever. It may occur even if the 
temperature be but slightly elevated. The left ventricle is 
most markedly involved: its walls are pale, turbid, and 
exceedingly soft and flabby; its cavity is usually somewhat 
dilated. The muscle-fibres are seen filled with numerous 


254 MANUAL OF THE PRACTICE OF MEDICINE . 

fine granules obscuring the striae and the nuclei. There 
may be some infiltration of the interstitial connective tissue 
with round cells, and the nuclei of the muscle-cells are usu¬ 
ally swollen and multiplied. The degeneration may merge 
into fatty degeneration. The symptoms are those of acute 
diffuse myocarditis, and a differentiation from that disease 
by clinical symptoms and physical signs is impossible. 

3. Fatty Heart. —The term “fatty heart” is loosely 
applied to either of two distinct conditions, fatty infiltration 
and fatty degeneration. 

(1) Fatty Infiltration {Cor Adiposum).— In' general obesity 
the normal amount of fat covering the heart is much in¬ 
creased ; bands of fatty tissue may extend between the mus¬ 
cular fibres even to the endocardium and the papillary mus¬ 
cles. The muscular fibres maybe normal or atrophied, or they 
may undergo pressure-degeneration. The heart-wall is 
weakened and may dilate or rupture. Such fatty infiltration 
occurs with general obesity, usually between the fortieth 
and seventieth years, and is more common in men than in 
women. It may more rarely be seen in the conditions of 
old age and cachexia. 

The symptoms are indefinite. There is dyspnoea on exer¬ 
tion, due either to the general obesity or to enfeebled heart- 
power. The pulse is usually weak and rapid. There may 
be angina pains. Sudden death may occur from rupture of 
the heart. 

The physical signs are elicited with difficulty because of 
the increased thickness of the chest-wall. The area of car¬ 
diac dulness may be increased by the fatty deposit. The 
heart-sounds are weak; there may be a systolic murmur at 
the apex, from relative insufficiency of the mitral valve. 

The treatment is that of general obesity, by regulated diet 
and systematic physical exercise. 

(2) Fatty Degeneration .— Etiology. —The heart is very 


DEGENERATION OF THE MYOCARDIUM. 


255 


subject to this form of degeneration. By reason of its 
incessant activity the heart needs an abundant supply of 
oxygen, and it is the most susceptible muscle in the body 
to show changes in nutrition. Any cause, therefore, pre¬ 
venting an abundant supply of good blood, or preventing 
good circulation of blood within the heart itself, will be 
followed by degeneration. Moreover, the heart-muscle is 
most susceptible to bacterial and chemical poisons. 

{a) Failure of general nutrition in old age, in cachectic states, 
and in wasting diseases. Fatty degeneration occurs in acute 
and chronic anaemia, and is more common in those who lead 
a sedentary life. 

( b ) Failure in local nutrition. Fatty degeneration com¬ 
plicates chronic pericarditis with adhesions; dilatation of 
the heart, or heart weakness from any cause by which 
the circulation of blood in the coronary arteries is allowed to 
become sluggish by reason of feeble contractile power of the 
ventricular wall; aortic regurgitation, in which the dimin¬ 
ished arterial tension does not allow of efficient filling of the 
coronary arteries. It may occur in the hypertrophied heart 
of valvular disease. It is common with disease of the coro¬ 
nary arteries. As this latter condition is usually secondary 
to atheroma of the aorta, fatty degeneration of the heart 
should always be suspected in old people with atheromatous 
changes of the aorta and the aortic valves associated with a 
weakly-acting heart. 

(c) Poisoning of the heart-muscle. This complication may 
occur with severe infectious disease, especially diphtheria 
and typhoid fever, and may be associated with fatty degen¬ 
erations in other viscera. It is seen in an intense form 
after poisoning by phosphorus or by arsenic. It may be 
caused by long-continued intemperance, or it may occur 
with diabetes. 

Fatty degeneration occurs more frequently in men than in 


256 MANUAL OF THE PRACTICE OF MEDICINE. 

women, and is usually a disease of adult life or of old age. 
In some cases no assignable cause can be found. 

Pathology. —The process may be general or local. The 
left ventricle is usually, however, affected. At first there 
appear yellowish striae and points under the endocardium, 
especially in the papillary muscles and the trabeculae, the 
remainder of the myocardium being healthy. In more 
marked cases, such as are seen in profound anaemia, the 
entire heart may be of a light-yellowish color and be very 
feeble and flabby, the heart-muscle often tearing easily. 
There may be areas of a brownish color—the so-called 
“ brown atrophy.” This is especially seen in cases asso¬ 
ciated with valvular disease or senility. The heart-cavi¬ 
ties may be dilated, and in extreme cases may rupture. Micro¬ 
scopically, the muscular fibres are seen to be filled with 
fatty granules and oil-drops; the striae and the nuclei are 
indistinct. In severe cases the fibres seem completely occu¬ 
pied by the granules. The areas of brown atrophy, when 
present, show the color to be due to a deposit of yellow¬ 
ish-brown pigment about the nuclei. 

Symptoms. —In some cases sudden death occurs, with or 
without previous indications of cardiac trouble. Such a 
fatal event may follow the giving of ether or chloroform, 
sudden mental shocks or emotions, after exertion, or after 
a hearty meal. In other cases there are more definite 
symptoms. 

Usually symptoms of cardiac insufficiency appear. There 
may be dyspnoea on exertion, or it maybe constant. The pulse 
is short and unsustained. Such a pulse may be a constitu¬ 
tional peculiarity in some persons, but is suspicious if met with 
in old people. The pulse may be regular or irregular, fre¬ 
quent or slow, falling at times even to 8 or 10 to the min¬ 
ute. A slow pulse of low tension is characteristic when it 
occurs, but it is rather rare. The pulse may become rapid 


DEGENERATION OF THE MYOCARDIUM . 


25; 


and irregular, and may “go to pieces” upon exertion, 
whereas the pulse of functional disease of the heart becomes 
stronger and more regular on exertion. 

Extreme fatty changes, however, may be consistent with 
a full regular pulse and regular heart’s action, provided dila¬ 
tation of the heart does not occur. It seems, then, that 
the symptoms really depend upon the supervening dilata¬ 
tion. When dilatation occurs, there are the ordinary symp¬ 
toms of such condition. It can usually, however, be differ¬ 
entiated from dilatation from other causes by attention to 
the following points: (1) The heart is not always much 
increased in size. (2) The symptoms are more con¬ 
stant. (3) CEdema and anasarca are exceedingly uncommon. 
(4) There are frequently present symptoms of a certain diag¬ 
nostic value. They comprise symptoms of syncope, pseudo¬ 
apoplectic and epileptic seizures, and angina pectoris. 

The syncopal attacks are characterized rather by their 
duration than by their intensity. There is never entire loss 
of consciousness, but the attack may continue with feeble 
heart-action, frequently a pulse sinking to 30 or 40 to the 
minute, and cold, clammy skin for hours. Such an attack 
in an old person or in one in whom a sufficient cause for 
fatty degeneration is present is exceedingly significant. 

The pseudo-apoplectic attacks are characterized by the sud¬ 
den onset of coma with stertorous breathing, often of the 
Cheyne-Stokes variety. There may even be a temporary 
hemiplegia. Absence of raised arterial tension and of the 
characteristic temperature-curve differentiates this condition 
from cerebral hemorrhage. The attack is probably due to 
circulatory disturbances of the brain from a weakly-acting 
heart. From such an attack the patient may recover, but 
he is always mentally enfeebled. 

The epileptiform attacks resemble those of petit mal. 
There are convulsive movements, which are not usually 
17 


258 MANUAL OF THE PRACTICE OF MEDICINE . 

severe. The patient is partially unconscious, not as in epi¬ 
lepsy, but more as in syncope. 1 he pulse is usually slow, 
often as low as 20, and of low tension. There may be men¬ 
tal delusions or mania following such an attack. 

The angina attacks are identical with those of the true 
or the false angina. 

Physical Signs. —There are no essential physical signs 
in fatty degeneration. There need be no increase in the 
size of the heart, and no murmur unless from pre-existing 
valvular disease. There may, however, be evidences of 
dilatation consequent upon the fatty degeneration, and a 
systolic murmur at the apex, due to relative mitral insuffi¬ 
ciency. The heart’s impulse is weak, vibratory, or absent. 
The first sound is short—a suspicious sign in old people ; 
the sounds may be equidistant, and the gallop rhythm may 
be present. The absence of physical signs adequate to 
explain the symptoms of cardiac inefficiency is of the 
greatest aid in diagnosis. 

Prognosis. —Mild cases following anaemia, wasting 
diseases, and fevers usually do well. The symptoms are 
never well marked, consisting usually only of a rapid weak 
pulse and some little dyspnoea on exertion, with a tendency 
to syncopal attacks. The heart-muscle returns to a state 
of health when the general health of the patient improves. 

The prognosis of the severer forms is bad. Fatty 
degeneration occurring in a hypertrophied heart with valvu¬ 
lar disease weakens the muscular wall, allows of dilatation, 
and upsets compensation. Sudden death may occur at any 
time, either unexpectedly, as during an attack of syncope, 
pseudo-apoplexy, epilepsy, or angina, or from rupture of 
the heart. The patient may die from heart weakness 
should he be attacked with any intercurrent disease. 

Treatment. —The patient should avoid every physical or 
mental excitement that might tax the power of the heart. 


ANEURYSM OF THE HEART. 


259 


Rest is of the utmost importance. The diet should be 
simple and nourishing. The stomach should not be over¬ 
distended by food or by gas. The strictest attention is to 
be paid to the general health. Anaemia should be met with 
iron tonics ; malnutrition, by proper feeding, cod-liver oil, 
and fresh air. Wine with the meals may be allowed, to 
stimulate digestion. 

Symptoms of heart feebleness should be controlled by 
heart stimulants and strict enforcement of rest. Digitalis 
is often of great service, but any of the other cardiac tonics 
may be employed. Nitroglycerin is to be employed if the 
tension of the pulse be high from associated arterio¬ 
sclerosis. The general management of the case is that of 
valvular disease with broken compensation. Angina attacks 
are best relieved by amyl nitrite, nitroglycerin, or mor¬ 
phine given subcutaneously, while sudden attacks of heart 
failure require active stimulation by inhalations of amyl 
nitrite or ammonia or by hypodermics of ether, whiskey, or 
digitalis. 

ANEURYSM OF THE HEART. 

1. Aneurysm of a valve results from weakening of the 
valve by either simple or malignant endocarditis. Aneu¬ 
rysms of the aortic valve bulge into the left ventricle; those 
of the mitral valve, into the auricle. The aortic valves are 
most frequently affected, the anterior mitral segment being 
more often involved than the posterior. Rupture of a 
valve-aneurysm produces extensive destruction and incom¬ 
petency. 

2. Aneurysm of the heart-wall is preceded by weakening 
of the wall by chronic myocarditis, by endocardial ulcerations 
of malignant endocarditis, and by areas of anaemic necrosis. 
In rare cases aneurysm of the heart-wall has followed stab- 
wounds. The usual situation of an aneurysm is in the left 


260 manual of the practice of medicine. 

ventricle near the apex. Aneurysm of the auricles or of 
the right ventricle is rare. The aneurysm may vary in size 
from that of a nut to that of the heart itself. Its sac is 
composed of pericardium, myocardium (the muscular fibres 
of which are often replaced by fibrous tissue), and endocar¬ 
dium. The cavity of the aneurysm is frequently occupied 
by laminated fibrin. Rupture of the aneurysm has occurred 
in but 7 out of 90 cases. 

The symptoms are not distinctive, and a diagnosis is 
rarely made. There may be near the apex some localized 
bulging, which may give an expansile pulsation. If the 
aneurysm be large, there may be marked disproportion be¬ 
tween its pulsation and the feeble pulsation in the peripheral 
arteries. 

The prognosis is exceedingly grave. Death may result 
from syncope or rupture, but more usually it occurs grad¬ 
ually from heart exhaustion due to the primary disease. 

The treatment is that of fatty heart. Nothing can be 
done directly for the aneurysm. 

RUPTURE OF THE HEART. 

Etiology. —A degenerated condition of the myocardium 
must in all cases precede rupture of the heart. Fatty de¬ 
generation, especially of localized areas, is the most frequent 
cause, occurring in 77 per cent, of all cases, but anaemic 
necrosis following thrombosis of the coronary arteries, fatty 
infiltration, circumscribed myocarditis, broken-down tumors 
and gummata, and deep endocardial ulcerations and cardiac 
aneurysms may also lead to rupture. Two-thirds of all 
subjects of rupture of the heart are over sixty years of age. 
The rupture usually occurs after exertion, but it may occur 
while the patient is at rest. 

Pathology. —The usual situation of the rupture is in the 
anterior wall of the left ventricle, near the apex; more rarely 


PALPITA TION. 


261 


the rupture may be situated in the posterior wall of the left 
ventricle, in the septum, or in the wall of the right ventricle. 
The rupture is usually small, and it may be either direct or 
indirect. 

Symptoms. —If the rupture be direct, the patient experi¬ 
ences agonizing cardiac pain, suffocation, and great appre¬ 
hension. The pulse becomes rapid and feeble; the skin is 
cold and clammy. Death may occur in syncope in a few 
minutes (in 71 per cent, of cases), or it may be deferred for 
several hours. In the more protracted cases vomiting and 
purging may be noticed. 

The prognosis is always fatal. 

The treatment is entirely prophylactic. Persons known 
to have degeneration of the myocardium should lead tran¬ 
quil lives free from every mental or bodily strain. 


4. NEUROSES OF THE HEART. 

PALPITATION. 

The term “ palpitation ” is applied to all forms of abnor¬ 
mal cardiac sensations which are unpleasantly sensible to 
the patient. The destructive features are violent pulsations 
of an unpleasant nature, usually with throbbing of the larger 
arteries. The pulse may be rapid and over-forcible, but it 
may be normal or even weak. The attack appears suddenly, 
lasts a few minutes or hours, and, while not serious, occa¬ 
sions considerable alarm. Various neurotic symptoms— 
flushing of the face, sweating, eructation of gas, and the 
abundant passage of limpid urine—often accompany or fol¬ 
low the attack. 

Palpitation is a pure neurosis, which may, of course, 
occur in a healthy or a diseased heart. It is to be distin- 



262 MANUAL OF THE PRACTICE OF MEDICINE. 


guished from the over-action of organic disease in that it is 
not produced by exertion—in fact, is often dispelled by 
exercise—appears often at night while at rest, and is not 
accompanied by dyspnoea or other symptoms of cardiac 
distress. 

Pathology. —There is no lesion, but in long-continued 
cases hypertrophy or dilatation may result. 

Etiology. —The cause of palpitation of the heart is a re¬ 
flex inhibition of the vagus action that enables the accelera¬ 
tors to run away with the heart. The affection is common 
in women and in young adults, and is rarer in advanced age. 
It occurs in weak and nervous conditions, after sickness, 
in hysteria and neurasthenia, in excitable subjects, and at 
the climacteric. It is produced by unhealthy occupations 
and by vicious modes of life. It is common with over-use 
of tea, tobacco, or coffee. Flatulent dyspepsia is a prolific 
cause of palpitation, and it may occur as a reflex phenom¬ 
enon from gastric, intestinal, or ovarian irritation. The effect 
of emotions is well known. Palpitation of the heart is a 
symptom of exophthalmic goitre. 

The “ irritable heart of soldiers ” (DaCosta) is a form of 
palpitation caused by excitement and over-exertion, espe¬ 
cially if the thorax be compressed with shoulder-straps ; this 
condition is accompanied with some dyspnoea on exertion. 

TREMOR CORDIS. 

This condition, which is the opposite of palpitation, oc¬ 
curs occasionally in youth and more commonly in advanced 
life. It may occur in healthy hearts or in those enfeebled by 
myocardial degeneration. The attack comes without warn¬ 
ing; the heart “trembles” or “flutters,” while the pulse 
sinks to a tremulous thread. The attack lasts for a few 
seconds and terminates by a forcible cardiac beat. 

Tremor cordis is almost always due to flatulence or car- 


INTERMITTENT action.—tachycardia. 263 

diac distress, and is not produced by emotions. There is no 
accompanying faintness, although the attack occasions seri¬ 
ous alarm. 

The prognosis is perfectly good. 

INTERMITTENT ACTION. 

Intermittent action occurs whenever the heart misses a 
beat from time to time. Intermittency may be regular or 
irregular, habitual and constant or only occasional. It 
usually occurs after meals, as an evidence of flatulent dys¬ 
pepsia; it occurs after over-use of tea, coffee, or tobacco; it 
is common in gout, in uric-acid diathesis, in nervous and 
hypochondriacal conditions, and after bodily and mental 
shocks. A constantly intermittent action of the heart is 
common to many old people, and is of no serious sig¬ 
nificance. 

Intermittency often occurs with fatty degeneration of the 
heart, and is to be distinguished from reflex intermittency 
by getting the patient to exercise briskly. By such exer¬ 
cise the really weak heart goes to pieces, while the healthy 
but neurotic heart clears up. 

Intermittency associated with organic disease of the heart 
is often of serious omen, indicating that the contraction of 
the auricles is not sufficient to fill the ventricles, hence the 
ventricles wait until they are properly filled. 

TACHYCARDIA. 

A rapid pulse accompanies many morbid conditions, such 
as fevers, exhaustion, collapse, emotional conditions pro¬ 
ducing palpitation, pain, maniacal conditions, and the inges¬ 
tion of certain poisons, as alcohol, atropine, nitroglycerin, 
and over-doses of digitalis. A rapid pulse is physiological 
after exertion and in the newly-born, whose normal pulse 
ranges between 120 and 135. 


264 MANUAL OF THE PRACTICE OF MEDICINE. 


The term “ tachycardia,” or “ heart-hurry,” is more 
properly applied to a rapid heart-action, often reaching 200 
or more in the minute, the action being, moreover, usually 
feeble. Its distinguishing feature is the very little disturb¬ 
ance it gives, in contradistinction to the rapid pulse ot exoph- 



Fig. 18.—Sphygmogram from a case of tachycardia. Pulse-rate, 175. 


thalmic goitre, of palpitation, of exertion, and of cardiac 
failure. Tachycardia may be due to tumors pressing on 
the vagus trunk or to mitral stenosis. In later life it is an 
important sign of senile degeneration, and is an added source 
of danger, as the attack may terminate in syncope or in 
asystole. 

Reflex tachycardia, a pure neurosis, may occur from any 
source of irritation, especially from gastric distress, and in 
reflex tachycardia the pulse may be fairly forcible. 

Intermittent tachycardia is a rare disorder in which heart- 
hurry comes in attacks at varying intervals, each attack 
lasting a few hours. The pulse is rapid and weak, fre¬ 
quently over 200 to the minute, but usually the distress to 
the patient is but slight. The cause for such attacks is not 
definitely known. A permanent cure is rare, and the dis¬ 
ease may terminate fatally at any time. 

BRACHYC ARDIA; BRADYCARDIA. 

Two forms of slow heart are recognized—the false and 
the true. 

False bracliycardia , in which the pulse is slow but the 


































BRACHYCARDIA ; BRAD YCARDIA. 


265 


number of heart-beats is normal, is usually due to a dilating 
heart with myocardial degeneration, in which the dropped 
beats are due to weak or abortive systole. In some 
cases false brachycardia seems to be due to alternating hemi- 
systoles, each ventricle acting independently. 

True brachycardia occurs whenever both pulse and cardiac 
systole are abnormally infrequent. 

Infrequent pulse occurs in some people as a constitutional 
peculiarity; it occurs in hunger, and it is frequent in the 
puerperal state. Pathologically it occurs in a number of 
conditions: 

(1) In diseases of the medulla and in compression of the 
brain ; for example, in basilar meningitis, tumors of the brain, 
and cerebral hemorrhage. It occurs also with diseases and 
injuries of the cervical cord. 

(2) In degeneration of the heart-muscle. A slow pulse 
in the aged is highly significant of fatty heart. The pulse 
may fall to even 8 in the minute in these cases. 

(3) After the sudden lowering of peripheral resistance, as 
by bleeding or by the withdrawal of effusions in the chest 
or the abdomen. 

(4) After the critical fall of temperature in acute fevers, 
especially in pneumonia, typhoid fever, erysipelas, and acute 
articular rheumatism. 

(5) In poisoning by digitalis, alcohol, aconite, or lead. 
Infrequent pulse occurs regularly with jaundice. It is com¬ 
mon in uraemia. The poison may be from auto-intoxica¬ 
tion following digestive disturbances—a very common cause 
for brachycardia. Thus it is frequently observed with ulcer, 
cancer, or dilatation of the stomach. 

(6) Conditions of asphyxia. 

(7) Various conditions of melancholia. 

Brachycardia is most common with advanced life. The 

affection is usually of serious import, as in senile hearts it is 


266 MANUAL OF THE PRACTICE OF MEDICINE. 


very often dependent upon dilatation and myocardial de¬ 
generation. 

The treatment is that of the underlying cause. 

ANGINA PECTORIS. 

Definition and Synonyms.—Angina pectoris is a disease 
characterized by severe pain over the heart, by a sense of 
impending death, and in severe cases by disturbances in the 
action of the heart. Synonyms: Stenocardia; Breast-pang; 
Neuralgia of the heart. 

Etiology.—The disease, which is one of adult life, and 
usually of the higher classes, attacks men in over 80 per 
cent, of all the cases. The exciting cause of an attack may 
be either exertion, external cold, indigestion, or constipa¬ 
tion, subsequent attacks becoming more and more easily 
provoked. In some cases no exciting cause can be dis¬ 
covered. 

Lesion.—No one lesion is constant. Ossification or 
inflammation of the coronary arteries is commonly found. 
Fatty heart, arterial sclerosis leading to high arterial ten¬ 
sion, atheroma of the aorta or of the aortic valves, fibroid 
myocarditis, and chronic inflammation of the coronary 
plexus are also among the pathological findings. In some 
rare cases no lesion is discoverable. 

The nature of the disease is not well known, The best 
explanation seems to be that a sudden high tension occurs 
in the arteries, causing a spasm of the heart in its efforts to 
overcome the resistance. The same spasm occurs in an 
over-filled bladder or stomach when its contents cannot 
easily be expelled, causing often agonizing pain. As a 
matter of fact, extreme degrees of arterial tension occur in 
96 per cent, of all cases of angina pectoris during the 
attack. In the 4 per cent, of cases in which the tension 
is not raised no explanation can be given. There being 


ANGINA PECTORIS. 267 

in almost all cases some lorm of cardiac lesion, angina 
pectoris affords the strongest presumptive proof of organic 
disease. 

Symptoms.—The symptoms occur in attacks lasting 
from a few seconds to half an hour. One or two minutes 
is the average duration. The severer attacks occur at night. 

o 

Each attack is attended by three cardinal symptoms: 

(1) Pain over the heart is exceedingly severe; it is neur¬ 
algic in character, with a sense of constriction. The pains 
may radiate up the neck and down the left arm and hand, or 
they may extend to the back. The face is cold, ashen-pale, 
and clammy; the expression is anxious; there may be 
general sweating. The patient immobilizes himself from 
pain. With the pain there may be a feeling of numbness 
or coldness in the fingers. 

(2) Dread of impending death coexists with the pain in 
an equal degree. After the attack is over the patient fre¬ 
quently exclaims that if the pain had lasted a minute longer 
he would have died. In attacks cut short by the use of 
drugs the sense of impending death may not be noted. In 
mild degrees the patient may complain only of uneasiness 
and general apprehension. 

(3) Disturbance m the heart's action occurs in almost all 
attacks. The pulse becomes rapid and irregular, and in 96 
per cent, ol cases is of extremely high tension. In some 
cases, however, the pulse may be uniform and but slightly 
altered. 

There may be considerable dyspnoea, and during the 
attack there may be a vehement desire to pass urine, 
although the bladder be empty. 

The attack may terminate in recovery, usually with the 
eructation of gas, with vomiting, or with the passage of a 
large quantity of limpid urine; or the patient may pass into 
syncope, from which he may or may not recover. 


268 MANUAL OF THE PRACTICE OF MEDICINE. 


Some patients who have had angina suffer from time to 
time from attacks of faintness without either pain or dread. 
This condition is not really angina, but is equally as 
serious. 

There may be but one attack of angina, or there may be 
a number of attacks at irregular intervals of weeks, months, 
or years. 

Between the attacks the disease itself gives no symptoms, 
although the underlying cardiac lesions present their 
ordinary clinical symptoms and physical signs. 

The prognosis is bad. The patient may die in many of 
the attacks, some patients not surviving the very first. Re¬ 
curring attacks, as a rule, become more frequent and more 
severe, although it is possible for the attacks at any time to 
cease recurring. Much can be done by judicious treatment. 
The prognosis is best in cases in which the attacks are 
induced by a preventable cause. The disease often runs a 
protracted course, and is not so serious if associated with 
aortic disease. 

Treatment .—During an Attack .—Treatment is directed 
toward the blood-tension and the pain. If the arterial 
tension be increased, amyl nitrite should at once be given 
by inhalation, from 2 to 5 drops being placed in cotton or 
on a handkerchief and applied to the nose. Patients 
subject to attacks of angina pectoris should carry with 
them constantly the pearls of amyl nitrite, and should use 
them at the first indication of an attack. Usually this 
treatment cuts short an attack, but it may fail. If relief is 
not afforded in a minute or two by amyl nitrite, chloroform 
should be given, a few inhalations often affording prompt 
relief. In some cases a hypodermic injection of morphine 
must be resorted to ; its action is rendered more efficient 
by a hot bath. In case the arterial tension be not increased, 
amyl nitrite does not do much good, and the treatment 


PSEUDO-ANGINA. 269 

consists chiefly in morphine combined with inhalations of 
chloroform. 

Between the Attacks .—The general health should be 
cared for in every possible way. Excitement and sudden 
or severe muscular effort should be avoided. Tobacco and 
stimulants are prohibited. Exciting causes of attacks 
should be found and prevented. If the blood-tension is 
high between the attacks, it should be reduced by regula¬ 
tion of the diet and the action of the kidneys and the 
bowels and by the use oi drugs. For this purpose nitro¬ 
glycerin may be given in gr. doses, at first three times a 
day, the dose being increased gradually until the patient 
complains of flushing or of headache. 

Prolonged use of iodide of potassium is often followed 
by good results. From 10 to 20 grains, three times a day, 
may be given for years, the dose being omitted from time 
to time or being replaced by doses of nitroglycerin to avoid 
iodism. There may be good results obtained by combining 
chloral hydrate in 5- or 7-grain doses with the iodide. 

PSEUDO-ANGINA. 

Etiology.—Women are more frequently affected with 
pseudo-angina than are men. The disease is most common 
in the nervous and neurasthenic, and is apt to be associated 
with other nervous and vaso-motor phenomena. It may 
occur at any age. It is common at the menopause, and may 
occur with especial frequency at the monthly sickness. The 
attacks may arise spontaneously, or they may be precipi¬ 
tated by worry or by disturbing emotions. In some cases 
there is a distant reflex origin. 

Pathology.—Pseudo-angina is a pure neurosis, and there 
is no essential lesion. 

Symptoms.—The disease comes in attacks which last 
for minutes, days, or even for weeks. If the attack be pro- 



270 MANUAL OF THE PRACTICE OF MEDICINE. 

longed the symptoms are remittent. The average duration 
is one or two hours, being longer than in true angina. 
The attacks, which may recur with a certain periodicity, are 
usually more frequent than in true angina. The symptoms 
of an attack somewhat resemble those of true angina. There 
is pain over the heart, which, however, is less severe, more 
diffused, and often is accompanied with precordial tender¬ 
ness. The patient does not immobilize himself as in angina, 
but is agitated and anxious. There is not the same dread 
of impending death, although the patient is apprehensive. 
The heart’s action is either feeble and irregular or tumult¬ 
uous. The arterial tension is not increased. The breath¬ 
ing is rapid and oppressed. Vomiting and pain over the 
stomach are common toward the close of protracted attacks. 
There may be various hysterical or neurotic symptoms dur¬ 
ing and between the attacks. 

The diagnosis is chiefly to be made from true angina. 
The chief points of diagnosis have already been given. The 
absence of arterial or cardiac lesions would be of importance 
in excluding the true angina. There are, however, difficult 
cases of combined hysteria, aortic valvular disease, and an¬ 
gina pains in young women, in which an absolute diagnosis 
cannot be made. 

The prognosis is perfectly good both for life and for 
recovery. 

Treatment.—During the attack the action of the heart 
should be regulated ; if the attack be prolonged, sedatives 
and anti-neuralgic remedies may be employed, such as 
phenacetine, bromide of sodium, and camphor or cannabis 
indica. As the arterial tension is not increased, amyl 
nitrite, nitroglycerin, and similarly acting drugs are not 
indicated. Between the attacks treatment should be directed 
toward the general health and the underlying nervous 
condition, 


EXOPHTHALMIC GOITRE. 


271 


EXOPHTHALMIC GOITRE. 

Definition and Synonyms.—Exophthalmic goitre is a 
disease characterized by enlargement of the thyroid gland, 
protrusion of the eyeballs, and tachycardia, together with 
various nervous phenomena. The disease was first de¬ 
scribed in 1786 by Parry, but a complete description was 
first given in 1835 by Graves of Dublin, and in 1840 by 
Basedow of Germany. Synonyms: Graves’ disease ; Base¬ 
dow’s disease. 

Etiology.—While no age is exempt, exophthalmic goitre 
is most common between the ages of fifteen and thirty-five. 
It occurs in women in the proportion of 5 to 1. When it 
occurs in men it seems to run a more severe course. It is 
most common in anaemic nervous people, and may run in 
families predisposed to nervous ailments. It may follow 
a blow, a shock, or a fall. It may occur after preg¬ 
nancy, although when pregnancy occurs in a patient af¬ 
fected by the disease, recovery more or less complete may 
ensue. 

Pathology.—The nature of the disease is unknown. A 
supposed lesion has been sought for in the sympathetic 
nervous system, but changes in the nerves and the ganglia 
are neither constant nor peculiar. The disease can be re¬ 
produced in dogs by destruction of the restiform bodies, 
and a case has been reoorted in which hemorrhages were 
found in the floor of the fourth ventricle. No one theory 
at present advanced explains all the symptoms of the 
disease. 

The symptoms of exophthalmic goitre may be divided 
into four groups : 

1. Heart Symptoms .—The heart’s action becomes rapid, 
running frequently as high as 120 to 140, or even 200, beats 
in the minute. The rapidity is largely controlled by the 


272 MANUAL OF THE PRACTICE OF MEDICINE. 

conditions of rest and exertion. The action of the heart is 
usually forceful and accompanied by a feeling of palpitation, 
but both these latter symptoms may be absent. The tachy¬ 
cardia is usually the first symptom observed, and, in fact, 
the disease may stop here, with this as its only symptom. 
There is usually marked pulsation of the carotids, and there 
may be a capillary pulsation. In long-continued cases there 
may be hypertrophy of the heart, which may in debilitated 
subjects merge into dilatation. Soft systolic murmurs at the 
base are common; they may be heard at the apex as well. 

2. Exophthalmos usually follows the tachycardia. The 
eyeball is protruded, and the eyelids do not cover the scler- 
otics, leaving a rim of white above and below the cornea, 
giving the patient a peculiar startled look. The protrusion 
may be extreme, so that the eye is dislocated from its 
socket. There is a lack of synchronism between the action 
of the eyeball and that of the upper eyelid, so that when 
the eyeball is moved downward the lid does not follow it as 
in health. This is known as “ Graefe’s symptom.” The 
upper eyelid may be so retracted that it is retained near the 
bony wall of the orbit, and to this condition is given the 
name of “ Stellwag’s symptom.” The pupils and the optic 
nerves are usually healthy, but pulsation of the retinal ves¬ 
sels is common. Exophthalmos may be absent in some cases. 

3. Goitre develops with the exophthalmos. It may be 
general or in only one lobe, and the enlargement is rarely 
so extreme as in simple goitre. The gland is soft and 
pulsating at first, becoming firmer and harder in protracted 
cases. There is usually a thrill felt on palpation. On 
auscultation may be heard a systolic murmur, or more 
commonly a venous hum. 

4. Nervous symptoms are common to almost all cases, but 
there is considerable variety in the extent to which they are 
developed. 


EXOPHTHALMIC GOITRE. 


273 


Emotional and mental disturbances are common. There 
may be hysteria, neurasthenia, irritability of temper, and 
mental depression often passing into melancholia. There 
may be temporary mania. There is a tendency to general 
neuralgic pains. Symptoms of general paresis have been 
observed in a few instances. 

Muscular tremors comprise one of the most constant 
symptoms of the disease. The tremor is usually fine, 
generally first involving the hands, and is more marked on 
motion. It may become general, and may even interfere 
with the walking power. In rare cases the tremor may be 
limited to one member. 

There is usually insomnia. There may be attacks of 
precordial pain resembling pseudo-angina. The skin is 
persistently moist with perspiration, and the electrical resist¬ 
ance of the body is diminished. 

Derangements of the digestion are common. There may 
be intermitting attacks of diarrhoea and flatulency, with 
severe and distressing vomiting resembling the gastric or 
gastro-intestinal crises of locomotor ataxia. There may be 
pigmentation of the skin as in Addison’s disease, or patches 
of leucoderma. The hair may become white or may fall 
out. Urticaria and angio-neurotic oedema of the skin are 
common. There may be slight irregular fever without 
known cause. 

Alternating flushings and pallor of the face with hot and 
cold flashes are common. Menstrual disorders frequently 
occur, amenorrhoea being the rule, although menorrhagia 
may occur. There may be paroxysmal dyspnoea occurring 
especially with the attacks of palpitation. 

Prognosis.—Exophthalmic goitre runs usually a chronic 
course extending over years. It is seldom fatal except from 
the dilatation of the heart that may be induced. A certain 
number of patients recover completely or in part, but when 
18 


274 MANUAL OF THE PRACTICE OF MEDICINE. 

the disease is well developed recovery is rare. There are 
some acute cases following fright in which recovery is 
rapid. 

Treatment.—The general nervous and anaemic condition 
should receive efficient treatment. The diet should be 
nutritious and digestible. Moderate exercise in the open 
air is to be enforced systematically if possible. All causes 
for nervous irritation should be avoided, and iron with 
arsenic or inhalations of oxygen gas should be given, 
together with general nervines and tonics. The action ol 
the heart should be regulated. Digitalis and strophanthus 
may succeed, but they are not reliable. Convallaria often 
does good when digitalis fails. Ergot may be employed 
with benefit, and belladonna given until dryness of the 
throat is obtained may be of service. Brilliant results often 
are obtained by iodide of potassium in 5- or 10-grain doses 
three times a day combined with from 10 to 15 grains of 
sodium bromide. This combination is especially indicated 
where the heart’s action is rapid and forceful with subjec¬ 
tive feelings of palpitation. 

Aconite and veratrum viride are not of much benefit. 
Rest in bed with cold applications (as an ice-bag or Leiter’s 
coil) over the heart are often efficient. In less severe cases 
a smooth piece of ice may be rubbed briskly over the heart 
for fifteen minutes two or three times a day. 

The use of galvanism has been recommended highly, 
and it should always be tried as a routine measure. The 
cathode should be placed at the back of the neck or at the 
angle of the jaw, while the anode is placed over the course 
of the sympathetic in the neck or over the heart. An 
application for fifteen minutes every second day is suf¬ 
ficient. 

Feeding with raw thyroid glands of the sheep and 
hypodermic injections of thyroid extract have been em- 


CONGENITAL MALFORAIA T/ONS. 


2/5 


ployed, but with unfavorable results. In severe cases 
thyroidectomy may be resorted to with a fair percentage of 
cures and improvements; but the operation is in itself a 
considerable source of danger. Ligation of the thyroid 
arteries has been recommended. 


5. CONGENITAL MALFORMATIONS. 

Congenital malformations may be due to arrested or 
abnormal development or to endocarditis during fetal life. 
The following classification is the one generally adopted : 

Patency of the Foramen Ovale.—If the patency exists 
in but small degree, it is not of serious importance unless 
accompanied by other anomalies. The greater degrees 
of patency are not incompatible with fairly prolonged 
life. In these cases the diagnosis can be suspected by 
marked cyanosis, either without heart-murmurs (fairly 
diagnostic) or by systolic and presystolic murmurs heard 
over the mid-sternum at the level of the third and fourth 
ribs. 

Defects of the Septa.—Minor defects of the ventricular 
systole are not rare and are not of much importance. 
Major defects rarely occur alone, but usually are associated 
with stenosis of the pulmonary valve, forming a most 
serious lesion. The defect results in the propulsion of 
blood from the stronger left ventricle into the right heart 
during systole, leading to embarrassed respirations and 
venous congestions. The physical sign is a loud systolic 
murmur heard over the whole precordium and between the 
shoulders, and not transmitted. Both auricular and ven¬ 
tricular septa may be defective, producing the cor bilocu- 
lare , or the reptilian heart. 

Stenosis or Incompetence of the Tricuspid and Mitral 



276 MANUAL OF THE PRACTICE OF MEDICINE . 

Valves. —These defects are rare. For physical signs see 
Chronic Endocarditis, pp. 223-249. 

Stenosis and Atresia of the Pulmonary Orifice or of 
the Conus Arteriosus. —These affections comprise the 
most important group of cases, being, moreover, relatively 
common. Pulmonary stenosis alone is not inconsistent 
with life for some years. For the physical signs see 
Pulmonary Stenosis, p. 243. The lesion, however, is usually 
associated with defects of the ventricular septum, and the 
prognosis is thereby rendered far more serious. 

Persistence of the Ductus Arteriosus. —This channel 
should normally be closed on the fourteenth day. If 
patent, there result rapid hypertrophy and dilatation of the 
right ventricle, dilatation of the pulmonary artery, dyspnoea, 
cyanosis, and congestion of the lungs, with general venous 
congestions. The physical signs are a long-continued 
systolic murmur over the pulmonary area, a systolic thrill, 
and a protrusion of the upper part of the sternum. 

Stenosis of the Aortic Orifice. —Stenosis of the aorta is 
rare. It is a serious lesion, incompatible with life for more 
than a few weeks. Stenosis of the conus arteriosus is not 
inconsistent with a fairly prolonged life. The circulation is 
carried on by anastomoses between branches of the sub¬ 
clavian with those of the epigastric and intercostal arteries. 
The arteries of the upper extremities are regularly larger 
and fuller than those of the lower. 

Transposition of Arterial Trunks. —This condition is 
necessarily fatal in utero , unless compensated by other 
anomalies, such as open foramen ovale or communication 
between the pulmonary vein and the right side of the heart. 

Numerical Anomalies of the Valve-segments.—Super¬ 
numerary valves are of no significance. Deficiency of 
valve-segments is usually associated with other and more 
serious anomalies. 


DISEASES OF THE ARTERIES . 


2 77 


Ectopia cardis may occur with congenital fissure of the 
sternum and abdomen. Displacement of the heart into the 
neck or the abdomen may occur. There may be acardia, 
double heart, bifid apex, or absence of the pericardium. 

Symptoms. —Radical defects are inconsistent with life, 
so that the child dies m ntero or shortly after birth. In 
those who live cyanosis is so marked a feature that the 
name “ morbus caeruleus ” has been given to the disease, 
and the term “ blue babies ” has been applied to these 
children. The cyanosis, which may be constant or may be 
induced only by exertion or by crying, varies from a lead 
color to a purplish hue. The child shows retarded mental 
and physical development. The nails are clubbed. The 
external temperature is low, and there is a great suscepti¬ 
bility to cold. Pulmonary affections are common, dyspnoea 
and cough are frequently observed, and the child is apt to 
succumb to an attack of bronchitis or of pulmonary con¬ 
gestion, or to any of the ordinary diseases of childhood. 

Treatment consists in guarding the child from cold and 
in checking promptly intercurrent diseases. The treatment 
for the heart itself is the same as that for valvular disease 
of adults. 


6 . DISEASES OF THE ARTERIES. 

ARTERIO-SCLEROSIS. 

Etiology and Synonyms. —Arterio-sclerosis occurs as a 
disease of advanced age, usually in those over forty. It is 
one of the conditions of senility. Predisposition to arterial 
degeneration runs in some families and may be inherited. 
Among the exciting causes are chronic alcoholism, lead¬ 
poisoning, gout, syphilis, diabetes, and over-eating, espe¬ 
cially with sedentary habits of life. There may be an ante¬ 
cedent history of uric-acid diathesis. The disease is common 



278 MANUAL OF THE PRACTICE OF MEDICINE. 

with chronic articular rheumatism, and may precede, follow, 
or develop simultaneously with Bright’s disease, especially 
with the granular kidney. It may follow severe over-work 
of the muscles. Synonyms: Chronic endarteritis; Atheroma. 

Pathology.— The aorta is almost always affected; next 
in frequency come the larger arteries. The disease may be 
uniformly distributed, or it may involve some arteries and 
not others; it may be either circumscribed or diffuse. The 
intima is much thickened by an increase of connective 
tissue and by the deposit of round cells. These cells may 
undergo fatty degeneration, imparting a yellow color in 
patches to the interior of the artery. In the deeper tissues 
the cells may break down to form a mixture of fat, detritus, 
and cholesterin-crystals from which the name “ atheroma,” 
or “ pulp,” is derived ; or, if near the surface, an atheroma¬ 
tous ulcer is formed. Atheromatous patches and ulcers and 
the narrowed lumen allow' of the formation of thrombi. In 
other cases the intima becomes markedly sclerotic and of 
bony hardness from the deposit in it of salts of lime. The 
media and the adventitia may show similar changes, even 
to fatty degeneration and calcification, or the media may 
become atrophied. 

Secondary lesions are found chiefly in the heart. The 
arterial lesion produces loss of elasticity, and consequently 
increases peripheral resistance to the work of the heart. 
The thickening of the intima may, moreover, cause such a 
narrowing of the lumen of the vessels that an added resist¬ 
ance results; in consequence, the left ventricle becomes 
hypertrophied in all cases in wdiich the nutrition of the 
patient is good, and compensation is effected. Should 
general nutrition fail, dilatation will ensue. 

The hypertrophied heart, pumping blood into the vessels 
whose outflow is impeded, raises arterial tension generally 
and causes an accentuation of the second aortic sound. 


ARTERIOSCLEROSIS. 


2/9 


The changes in the aorta may so weaken its wall as to 
allow the formation of an aneurysm. For the same reason 
miliary aneurysms may be formed in the cerebral arteries 
and may result in rupture and cerebral hemorrhage. 

Dry gangrene of the extremities may result from dimin¬ 
ished supply of blood from the narrowing of the arterial 
lumen by connective tissue or thrombi. 

Associated Lesions .—Contracted kidney occurs in the 
great majority of cases. It is often difficult to decide in a 
given case whether the arterial or the renal disease has 
been primary. 

Emphysema with chronic bronchitis is present in a large 
number of cases, and the patient is liable to have cirrhosis 
of the liver, as alcoholism is a common factor in cirrhosis 
and in arterial sclerosis. Atheroma of the aortic valves is 
a frequent complication. 

The symptoms are exceedingly diverse, depending upon 
which arteries are most affected and upon the secondary 
and associated lesions. Arterial sclerosis with compensa¬ 
tory hypertrophy is not inconsistent with general good 
health. When compensation fails the general symptoms of 
dilatation and heart-inefficiency occur. 

Sclerosis of the coronary arteries may produce throm¬ 
bosis with sudden death, fibroid degeneration, aneurysm or 
rupture of the heart, and angina pectoris. 

Cerebral symptoms are those of cerebral endarteritis 
(which see), comprising acute and chronic degeneration, 
spasm of cerebral vessels with transient or permanent 
paralyses, and cerebral hemorrhages. 

Renal symptoms may be absent, or the urine may be 
increased in quantity and of low specific gravity, with but 
occasionally hyaline casts and a trace of albumin. In 
other cases the renal symptoms are distinctly uraemic and 
may terminate the life of the patient. 


280 manual of the practice of medicine. 


The course of the disease may be complicated by aneur¬ 
ysm, by gangrene, or by an associated emphysema. 

Physical Signs.— The combination of increased arterial 
tension, hypertrophy of the left ventricle, accentuation of 
the second aortic sound, and an appreciable thickening of 
the arteries affords conclusive proof of the existence of 
arterio-sclerosis. A high-tension pulse may exist with 
very little sclerosis, but sclerosis and high tension usually 
go together except when the left ventricle fails. The pulse- 
wave is slow in its ascent, is felt for an appreciably long 
period, subsides slowly, and between the beats the pulse 



remains firm and full. The wave-fluctuations are compara¬ 
tively small. It is difficult, even impossible in some cases, 
to obliterate the pulse by firm pressure on the artery. The 
sphygmographic tracing (Fig. 19) shows a short slanting up¬ 
stroke, a flat or rounded summit, and a gradual descent in 
which the dicrotic wave is slighly marked or absent. 

The prognosis, so far as life is concerned, is not unfavor¬ 
able. The danger of renal or cardiac disease or of cerebral 
complications is always present. The chief question is 
whether compensatory hypertrophy of the left ventricle can 
be maintained. Sudden death may occur. 

Treatment.—Much can be done to limit the extension of 
the disease by a quiet mode of life, plain, non-stimulating 
diet, and a correction of those conditions known to pro¬ 
duce the disease. The state of the bowels and of the urine 








ARTERITIS 


Plate 16 



Small artery: thickening of all the coats (Delafield) 











ARTERITIS. 


Plate 17. 



Small artery: obliterating endarteritis (Delafield). 







ARTERITIS 


Plate 18 



Syphilitic endarteritis (Finger) : b shows thickened ultima 








s YPHIL /TIC AR TERITIS.—ANE UR YSM. 2 8 I 

should be regarded, and the skin should be kept active by 
daily baths. Alcohol is to be prohibited. High blood- 
tension should be reduced by appropriate drugs. Of these, 
nitroglycerin is the most serviceable, given in doses of gr. 
TFo every three or four hours, or at longer intervals if not 
well borne. Iodide of potassium in gr. x doses t. i. d. is of 
service, especially in syphilitic patients. It is advantage¬ 
ously combined with choral in gr. v-x doses. Sudden and 
severe muscular efforts should be avoided, especially if the 
aorta be extensively involved. When the heart begins to 
dilate, stimulants will be required. Digitalis should not be 
given, however, unless its effect in raising arterial tension 
be balanced by its combination with nitroglycerin. Should 
acute dilatation occur, with lividity and dyspnoea, venesec¬ 
tion may be resorted to. 

SYPHILITIC ARTERITIS. 

Besides syphilis being a causative factor in arterio-sclerosis 
and aneurysm, two specific forms of arteritis are described : 

1. Obliterating endarteritis with proliferation of new tissue 
within the intima, obstructing the lumen. There is also 
a small-celled infiltration of the middle and external coats. 
This form of infiltration is not absolutely characteristic of 
syphilis, but should be so regarded should other syphilitic 
changes be found. 

2. Gummatous Peri-arteritis .—Gumma develop within 
the adventitia, forming ovoid swellings along the course 
of the artery. There is usually an associated obliterating 
endarteritis. This process is distinctive of syphilis, and 
occurs especially in the coronary and cerebral arteries. 

ANEURYSM. 

The following forms of aneurysm occur: 

i. True aneurysm, in which the sac is formed by the 



232 MANUAL OF THE PRACTICE OF MEDICINE. 


arterial coats. The aneurysm may be cylindrical, fusiform, 
or sacculated. 

2. False or dissecting aneurysm, in which, from laceration 
of the intima, blood makes its way between the layers and 
may rupture through the outer coats. 

3. Arterio-venous aneurysm, where a communication ex¬ 
ists between an artery and a vein. If there be an interven¬ 
ing sac, the term varicose aneurysm is applied ; if the com¬ 
munication be direct, the condition is termed aneurysmal 
varix. 

Etiology. —There is always some weakness of the arterial 
wall, so that it becomes dilated from the blood-pressure. 
There is almost regularly arterial sclerosis, and the con¬ 
ditions which produce this sclerosis are therefore causative 
factors of aneurysm. Bacterial intection of the aortic wall, 
producing aneurysm, has been observed with malignant 
endocarditis. 

Embolism may lead to aneurysm by causing local degen¬ 
eration or injury of the vessel-wall. 

The determining cause of aneurysm is high arterial pres¬ 
sure from the arterial sclerosis or from severe muscular 
efforts. Aneurysm is more common in men than in women, 
and is more frequent among the working classes, as long¬ 
shoremen, in whom alcoholism, syphilis, and over-work are 
important factors. It is rare before thirty and after fifty 
years of age, because arterial sclerosis does not appear be¬ 
fore the earlier limit, and because muscular strain is not so 
common after the latter age. 

Pathology. —The cavity of the aneurysm usually contains 
clots of blood, frequently laminated and partly organized. 
There may be calcareous degeneration of the clot. The 
vessels leading from the artery at the site of the aneurysm 
may be occluded; portions of the clot may become de¬ 
tached and carried into the circulation as emboli. Organ- 


ANEURYSM. 283 

ization of the clot is conservative in its nature and is more 
common in sacculated aneurysm. 

The aneurysm-wall is never composed of normal vessel- 
wall. The intima shows marked changes of arterial sclero¬ 
sis. The media is changed, and is often in a condition of 
fatty degeneration. The adventitia is thickened by inflam¬ 
matory processes, thus reinforcing the weakened arterial 
wall. The intima and the media may atrophy so that the 
wall consists of the adventitia alone. 

Aneurysms vary in size from microscopic miliary aneur¬ 
ysms to those the size of a child’s head or larger. 

Aneurysms may rupture, may compress neighboring 
organs, and may cause pressure-erosion. 

The situation of aneurysms varies. In 860 cases ana¬ 
lyzed by Sibson, the situation of the aneurysm was as 
follows: The ascending portion of the arch, 141 ; the 
transverse portion of the arch, 120; the ascending and 
transverse portions together, 112 ; the sinuses of Valsalva, 
87; the descending portions of the arch, 72 ; the transverse 
and descending portions together, 20; the whole arch, 28; 
the thoracic aorta, 71 ; the abdominal aorta at the cceliac 
axis, 131 ; the lower part of the abdominal aorta, 26. 

Symptoms.— An aneurysm, being a pulsating tumor in 
the course of the arterial circulation, growing in the stiff- 
walled thorax, and having a tendency to rupture, naturally 
produces four groups of symptoms: (1) The presence of a 
growing pulsating tumor; (2) its pressure on surrounding 
parts; (3) its effect upon the circulation of the blood; 
(4) the symptoms due to erosion and rupture. 

Symptoms of Aneurysm of the Thoracic Aorta.— 
Pressure-symptoms are usually marked, and afford data for 
the localization of the aneurysm. 

1. Pressure on the Vena Cava or its Branches .—There 
may be congestion and oedema of the arm and the face on 


284 MANUAL OF THE PRACTICE OF MEDICINE. 

one side, more rarely on both; or in old-standing cases 
there may be a brawny swelling of the base of the neck, 
termed by the French “ the collar of flesh.” Large aneur¬ 
ysms of the ascending aorta sacculated downward may press 
on the inferior vena cava, causing oedema of the feet and 
ascites. There may be erosion from pressure and rupture 
into the superior vena cava with aneurysms of the ascend¬ 
ing arch. Congestion of the chest-wall occurs from pres¬ 
sure on the azygos vein. 

2. Pressure on the Trachea and the Bronchi .—Moderate 
pressure causes symptoms of inflammation and cough with 
expectoration which may contain blood. More marked 
pressure on the trachea causes inspiratory dyspnoea, either 
steady or paroxysmal, or orthopncea. Ihere are developed 
symptoms of gradual asphyxia. In some cases sudden 
fatal asphyxia may occur either from pressure-erosion of a 
tracheal ring, allowing the trachea to collapse suddenly 
like a membranous tube, or from the lodgement of a plug 
of mucus at the pressure-point, causing total obstruction. 
Tracheal compression is usually seen with aneurysms of 
the transverse arch. Compression of a bronchus causes 
localized bronchial catarrh with sibilant and sonorous 
rales, dyspnoea, and diminished breathing over that part of 
the lung. There may be bronchiectasis and suppuration 
of the lung. The left bronchus is the one more frequently 
compressed. With large aneurysms the lung may be par¬ 
tially compressed. 

Rupture may occur into the lung, the trachea, or the 
bronchi. A large hemorrhage will cause death by anaemia, 
or, filling the bronchi, cause asphyxia or septic broncho¬ 
pneumonia. Small repeated hemorrhages may occur from 
moderate leakage. Aneurysms of the descending arch 
often rupture into a pleural sac. 

3. Pressure on the oesophagus occurs with aneurysms of 


ANEURYSM. 


285 


the descending aorta, more rarely with those of the trans¬ 
verse arch. Dysphagia may be either steady or parox¬ 
ysmal, and may lead to great emaciation. The case may 
resemble one of oesophageal stricture, and care should 
always be taken in such cases to exclude thoracic aneur¬ 
ysm before passing an oesophageal bougie, as otherwise 
instrumental rupture of the aneurysmal sac may result. 
Rupture into the oesophagus may occur and may be the 
first symptom of an unsuspected aneurysm. 

4. Pressure or Traction on the Recurrent Laryngeal 
Nerve. —The left side is more commonly affected. There 
may result spasm or paralysis of one or of both vocal 
cords. There is dyspnoea which is steady or paroxysmal; 
a brassy or clanging cough quite distinctive; husky or whis¬ 
pering voice or aphonia. Spasmodic dyspnoea of laryngeal 
origin is differentiated from obstructive dyspnoea of tracheal 
pressure by being relieved by inhalations of chloroform. 

5. Pressure on the Sympathetic Nerve. —In the early 
stages the pupil on the affected side is dilated and the skin 
is paler than normal; later occur contraction of the pupil 
and flushing and sweating of the skin. 

6. Pressure on the brachial plexus causes neuralgic pains, 
twitchings, and later areas of anaesthesia. 

J. Pressure on the Bones. —Pressure on the vertebrae 
causes the erosion of their bodies with a steady boring pain 
in the back that is distinctive of aneurysms of the descend¬ 
ing aorta. Complete erosion will expose the spinal cord to 
pressure with the symptoms of a transverse myelitis. 

8. Pressure on the intercostal nerves causes neuralgic pain. 
Pressure on the sternum and the ribs is common with aneur¬ 
ysms of the ascending arch. Boring pain is experienced, 
and there is apparent a large pulsating tumor covered finally 
only by red shiny skin resembling that of a pointing ab¬ 
scess. External rupture is the inevitable result. 


286 MANUAL OF THE PRACTICE OF MEDICINE. 


9. Aneurysms at the root of the aorta frequently cause 
angina pains. 

Physical Signs. —Inspection in many instances is negative. 
There may be bulging of the chest-wall, best appreciated 
with oblique light. This bulging occurs usually above the 
third rib, to the right of the sternum. Aneurysms of the 
ascending aorta are found projecting in the left scapular 
region. An external tumor may be formed by the sac 
approaching the surface, invading the intermediate struct¬ 
ures. The heart’s apex is often displaced downward and 
to the left. 

Palpation reveals an expansile pulsation of the tumor. 
There may be a heaving impulse without the appearance of 
an external tumor. There may be a systolic thrill, and in 
some cases a diastolic shock which is highly distinctive. 
Fluctuation may be detected when the sac has perforated 
the chest-wall. Care should be taken, however, in manipu¬ 
lation to avoid rupture of the sac. There may be pulsation 
in the sternal notch in case of aneurysm of the transverse 
arch. 

Percussion reveals dulness or flatness whenever the aneur¬ 
ysm is large enough to approach the chest-wall. Small, 
deeply-seated aneurysms do not, therefore, yield dulness. 
Dulness on the right side of the manubrium indicates aneur¬ 
ysm of the ascending arch ; dulness in the middle line ex¬ 
tending to the left points to aneurysm of the transverse arch; 
while dulness to the left of the spinal column occurs with 
aneurysm of the descending aorta. There may be tender¬ 
ness on percussion, and a sense of abnormal resistance. 

Auscultation may yield negative results even with large 
aneurysms. There may be a continuous hum louder at each 
systole, or a systolic or double murmur. The aortic second 
sound is usually accentuated, or it may be replaced by 
the murmur of an associated regurgitation at the aortic 


ANEUR YSM. 


287 

valve. There may be a systolic murmur heard over the 
trachea, due to the expulsion of air at each pulsation of 
an overlying aneurysm. 

The pulse in the arteries beyond the aneurysm is fre¬ 
quently altered, becoming 
slowed and the wave being 
partially effaced. 

Aneurysms of the ascend¬ 
ing arch alone, delay all 
pulses equally. Large an¬ 
eurysms of the descending 
aorta may totally efface the 
pulse-wave in the abdominal 
aorta and femorals. When 
the aorta at the origin of the 
innominate artery is involved, 
the right radial pulse is more 
retarded and effaced than the 

fgfh When the transverse ^^rta, showing shape of the outline and the 
. position of the customary double murmurs. 

arch is involved beyond the 

innominate, it is the left pulse that is the more affected. 

Tracheal tugging is a sign of much value in detecting 
deep aneurysms pressing backward upon the trachea or the 
left bronchus. The patient should sit with the chin de¬ 
pressed, so as to relax the tissues of the neck. The exam¬ 
iner, standing behind the patient, raises the cricoid cartilage 
on the tips of the index fingers. If an aneurysm be present 
in the situation above noted, a characteristic downward tug¬ 
ging will occur with each pulsation. This tugging is a sign 
of great value, although not absolutely pathognomonic. 
The heart may be displaced downward and to the left. It 
is not usually enlarged unless from some coexisting lesion. 

Diagnosis. —Throbbing of the aorta in aortic insufficiency, 
and displacement of the aorta forward with spinal curvature, 






288 MANUAL OF THE PRACTICE OF MEDICINE. 


may simulate aneurysm, but pressure-symptoms, pain, and 
retardation of the pulse are absent. Sacculated empyema 
receiving impulses from the heart may cause a pulsating 




Fir. 21.—Sphygmograms of the radial pulse on the right ( a) and the left side ( 3 ), from a 
case of aneurysm of the transverse part of the arch of the aorta. 

tumor, but the pulsation is not expansile, there are no cir¬ 
culatory symptoms, and septic symptoms occur. 

Pulsating sarcoma and other growths of the mediastinum 
often present great difficulties in diagnosis. The pulsations 
in these growths are not expansile, as in aneurysm, have less 
force and power, and have no diastolic shock. In some 
cases a differential diagnosis between a pulsating tumor 
and an aneurysm is impossible. 

The prognosis is always grave. Recovery may occur, 
but it is not to be expected. The aneurysm may rupture at 
any time, and the rupture may even be the first symptom. 
Dissecting aneurysms just above the sinuses of Valsalva 
rupture usually into the pericardium, causing sudden death. 
Sudden heart failure is common with aneurysm without 
rupture, and death may result from obstructive dyspnoea, 
myelitis, dysphagia, and exhaustion, or from associated 
endocarditis of the aortic valves. The course of the disease 





























ANEURYSM. 


289 

is usually about two years, although life may be prolonged 
in some cases for five or ten years. 

The treatment of aneurysm of the thoracic aorta consists 
in the attempt to secure coagulation within the sac. Rest 
is an essential feature of the treatment, and should be as 
nearly absolute as possible. Mental excitement of all kinds 
should be avoided. Tufnell’s treatment consists in the 
enforcement of rest and a restricted diet. He allows for 
breakfast 2 ounces of bread and butter with 2 ounces 
of milk; for dinner, 2 or 3 ounces of bread and 2 or 3 
ounces of meat, with from 2 to 4 ounces of milk or claret; 
for supper, 2 ounces of bread and 2 ounces of milk. This 
plan succeeds best in small sacculated aneurysms. Few 
patients, however, can stand such a radical reduction 
of food, so this treatment cannot be enforced rigor¬ 
ously. A more liberal supply may be given, but fluids 
should be restricted as much as possible. Systematic bleed¬ 
ing may prove of service in the earlier stages in robust sub¬ 
jects : 8 or 10 ounces of blood may be abstracted every 

ten days or two weeks, provided that excessive anaemia is 
not produced. 

Of medicines, iodide of potassium is most commonly em¬ 
ployed, the aim being to tranquillize the circulation and 
reduce blood-tension without increasing the frequency of the 
pulse. To find the proper dose the patient should be put to 
bed for several days, to find the rapidity of the pulse at rest. 
Then the iodide is to be given in 5-grain doses, well diluted, 
three times a day, and gradually increased as long as the 
pulse is not made more frequent. Rarely more than 10 
or 15 grains three times a day are necessary. One marked 
effect of the iodide is the reduction of pain. 

Aconite may be used for temporary over-action of the 
heart, but its administration for any length of time is not 
recommended. 


19 


29O MANUAL OF THE PRACTICE OF MEDICINE. 

Various forms of local treatment have been recommended, 
but with indifferent success. The insertion of horse-hair, 
catgut, wire, and the injection of styptics into the sac have 
been tried. Loreta’s method has been followed in some 
cases by good results. This treatment consists in filling the 
sac with fine silver wire pushed through a hypodermic 
needle, combined with electrolysis. 

Special symptoms are to be treated as they arise. Dysp¬ 
noea and congestion may be relieved by timely venesection. 
Morphine is to be employed for pain. Urgent dyspnoea 
may seem to indicate a tracheotomy, but the operation is 
usually useless, as the obstruction is below the site of the 
operation in nearly all cases. If chloroform inhalations re¬ 
lieve the dyspnoea, and if laryngoscopic examination reveals 
bilateral abductor paralysis, the operation may be resorted 
to. External rupture is to be retarded by painting the sur¬ 
face with a solution of gutta-percha, by the use of ice-bags, 
or by a metal or an elastic support. 

ANEURYSM OF THE ABDOMINAL AORTA. 

The usual situation of aneurysms of the abdominal aorta 
is near the coeliac axis, which is frequently involved. The 
aneurysm maybe fusiform or sacculated, and may be multiple. 
It may project backward, eroding the vertebrae, or it may 
project forward, attaining considerable size. It may rupture 
into the pleura, the retroperitoneal tissues, the peritoneum, 
or the intestines. 

Symptoms.— Pain is the most prominent symptom; it 
may be sharp, shooting, radiating down the legs, or it may 
be the steady boring pain of bone-erosion. Gastric symp¬ 
toms are common, especially gastralgia and vomiting. Em¬ 
bolism of the mesenteric artery may occur, producing severe 
colicky pain. Paraesthesia and paraplegia may result from 
pressure on the cord. 


ANEURYSM OF THE ABDOMINAL AORTA. 


2 91 


Physical Signs. —There may be a pulsating tumor ap- 
paient on inspection. By palpation a tumor of expansile 
pulsation is appreciated. There may be heard a systolic, 
diastolic, or double murmur. The pulse in the femorals is 
letarded and may be obliterated. To avoid mistaking a 
throbbing aorta for aneurysm, Osier says, “ It is to be 
remembered that no pulsation, however forcible, nor the 
presence of a thrill or a systolic murmur, justifies the 
diagnosis of abdominal aneurysm unless there is a definite 
tumor which can be grasped and which has an expansile 
pulsation .” A tumor of the pylorus with an impulse trans¬ 
mitted from the underlying aorta may be mistaken for 
aneurysm, but the impulse is not expansile and is lost when 
the patient assumes the knee-chest position, the tumor fall¬ 
ing forward away from the aorta. 

The prognosis of abdominal aneurysm is grave, although 
recovery is not impossible. 

The treatment generally is that of thoracic aneurysm. 

I ressure on the proximal portion of the aorta may be 
resorted to under chloroform. Pressure should not be too 
severe, as bad results have followed the bruising of the sac. 


III. DISEASES OF THE RESPIRATORY 

SYSTEM. 


i. DISEASES OF THE LARYNX. 

SPASM OP THE LARYNX. 

Two forms of spasm of the larynx are recognized: 
(i) Laryngismus stridulus; (2) Spasmodic laryngitis. 

1. Laryngismus Stridulus (Thymic Asthma). —This 
form occurs in children under two and a half years of age. 
Rickets is found in two-thirds of the cases. It is more 
common in boys, in delicate, dyspeptic, and nervous chil¬ 
dren. It is less frequent in America than in England, 
France, or Germany. It may be a symptom of tetany. 

Etiology. —The attack may be induced by any reflex 
cause for irritation, such as dyspepsia, poor air, constipa¬ 
tion, dentition, or attacks of crying ; it is favored by inflam¬ 
mation of any part of the respiratory tract. 

Pathology. —The disease consists of a spasm of the 
adductors of the larynx, without inflammatory basis. 

Symptoms. —The attacks may come at any time, but 
they are most common just as the child awakes. Respira¬ 
tion is suddenly arrested ; the child struggles for breath ; 
the face is pale, cyanotic, or congested; the pulse becomes 
weak and flickering; after a number of seconds the spasm 
relaxes and air is inspired with a loud crowing sound. 
During the attack there may be spasm of the hands and 
feet (“ carpopedal spasms ”), or even general convulsions. 
The attack is not accompanied by cough, hoarseness, or 
fever. The paroxysms may be as frequent in severe cases 
292 



SPASM OF THE LARYNX. 


293 

as thirty or forty during the twenty-four hours, and they 
may be continued at intervals for months. Slight reflex 
causes may at any time bring on the paroxysms. 

The prognosis is generally good, but it is possible for 
the child to die in any of the attacks. Severe spasms may 
be the cause of meningeal hemorrhage. 

Treatment.— The spasm is of such short duration that 
there is but little time for treatment. It seems best not to 
shake the child nor to dash water in its face, as has been 
recommended, but to keep the child quiet until the attack 
is over. Should the apncea be persistent, a hot bath (95 0 
F.) should be given and a cold compress be applied to the 
head. Intubation may be resorted to if danger be imminent. 

Recutrences of the paroxysms may be prevented by 
rectal injections of chloral hydrate (gr. ij-v) in milk of 
asafetida (oij), to which from 2 to 5 grains of sodium bromide 
may be added. Swollen gums should be lanced freely. 
The bowels should be regulated, and attention be paid to 
the propel scientific feeding of the child. Osier recom¬ 
mends warm baths two or three times a day while the back 
and the chest are being sponged with cool water. Any cause 
for reflex irritation should be discovered and properly 
treated. The importance of good fresh air and sunlight 
must be remembered in all cases. 

2. Spasmodic Laryngitis (Spasmodic Croup). —This is 
the more common form of spasm; it occurs regularly in 
children between two and five years of age, and equally in 
strong and in delicate subjects. 

Symptoms.—The attack comes regularly after the first 
heavy sleep, usually between 1 and 3 o’clock a. m. The child 
suddenly awakes and sits up in bed with evident dyspnoea. 
The inspirations are noisy, difficult, and “ croupythe 
voice is husky; there is a brassy “ croupy ” cough. The 
oppression and cyanosis may appear alarming, but after a 


294 MANUAL OF THE PRACTICE OF MEDICINE. 

time (from half an hour to an hour) the attack suddenly 
ceases and the child is as well as ever. During the attack 
there are neither constitutional nor inflammatory symptoms, 
and there is no fever. The attack may be repeated on sub¬ 
sequent nights, but in these cases there is usually added a 
mild catarrhal laryngitis, with cough, hoarseness, and possi¬ 
bly slight fever, during the day. 

The prognosis is perfectly good, notwithstanding the 

alarming appearance of the child. 

Treatment. —A prompt emetic should at once be admin¬ 
istered, such as wine of ipecac .3j, or mustard and water, 
the yellow sulphate of mercury (gr. ij—v) has been recom¬ 
mended, but as it may cause gastro-enteritis it should not 
be used. If the attack persist, hot baths and hot fomenta¬ 
tions to the throat may be employed. 

ACUTE CATARRHAL LARYNGITIS. 

Etiology. —Many cases of acute catarrhal laryngitis are 
due to catching cold or to breathing irritating and impure 
air, especially in patients with catarrhal affections of the 
nose and the throat. An attack may be induced by over¬ 
use of the voice. Laryngitis may be one of the lesions of 
“the grippe ” or of measles ; it may also complicate any dis¬ 
ease of the bronchi and lungs attended with cough and 
expectoration. It may also occur with any of the acute 
infectious diseases. 

Pathology.—On laryngoscopic examination the mucous 
membrane of the larynx is seen to be red, congested, and 
swollen. The inflammation may be generally distributed 
or it may involve only certain areas. The vocal cords are 
usually involved, and their mobility is impaired. There 
may be an over-secretion of the mucous glands, or only a 
slight mucoid exudation. Superficial ulcerations may re¬ 
sult in severe cases. In certain cases in adults there may 


ACUTE CATARRHAL LARYNGITIS. 


295 

be considerable oedema of the larynx, which may consti¬ 
tute a formidable complication. 

Symptoms.— In adults the course of the disease is 
somewhat different irom that in children. Fever may be 
slight or absent, but malaise to some extent is common ; 
slight rigors may initiate a severe attack. The voice be¬ 
comes hoarse or is reduced to a whisper; the cough is 
croupy or barking, and is usually paroxysmal and harass¬ 
ing. Pain referred to the larynx may be quite severe and 
steady; it is usually increased by swallowing, talking, or 
coughing. In other cases a burning, irritating feeling alone 
is complained of. Pressure over the cricoid cartilage may 
cause pain or a paroxysm of coughing. In severer cases 
with oedema of the glottis dyspnoea may be a marked symp¬ 
tom. The difficulty of breathing may be continuous or 
paroxysmal; it may lead to asphyxia. This complication is 
more common in those suffering from alcoholism and 
Bright’s disease. 

In Children .—The peculiarity of laryngitis in children is 
that it is often complicated by spasm of the larynx, consti¬ 
tuting a clinical group of symptoms to which the names 
“pseudo-croup” and “catarrhal croup ” have been given. 
This complication usually occurs in the winter months and 
in children under three years of age, although some chil¬ 
dren continue to have attacks until their tenth or twelfth 
year. The symptoms resemble those in adults, but they 
are more marked at night. The child is usually awakened 
by severe and distressing dyspnoea, not, however, of the 
same explosive violence that is seen in pure spasmodic 
laryngitis. The attack wears itself out in an hour or so, 
and the child is left with only the ordinary symptoms of 
laryngitis. 

The diagnosis must be made from spasmodic laryngitis 
and membranous croup. In spasmodic laryngitis the at- 


296 MANUAL OF THE PRACTICE OF MEDICINE. 

tack begins suddenly with explosive violence, and between 
the attacks the child is well and has no fever. In catarrhal 
laryngitis the child has been ailing, the dyspnoea begins 
more gradually, and between the attacks of dyspnoea the 
child has a cough, the voice is hoarse, and there is some fever. 

In membranous laryngitis the dyspnoea is more con¬ 
tinuous, the general symptoms are more severe, and there 
are usually patches of membrane on the pharynx and the 
tonsils. The cervical glands are also swollen. 

In adults laryngoscopic examination will make a positive 
diagnosis from nervous or hysterical aphonia and from sim¬ 
ple oedema glottidis. 

Treatment. —The patient should breathe warm, pure, 
and moist air, and must avoid over-use of the voice. Cold 
applications to the neck are often of great service. The 
following prescriptions are of use in allaying the cough: 

1 ^. Ammonii chloridi, oiss ; 

Mist, glycyrrhizae comp., 3iv.—M. 

Sig. A teaspoonful every two hours in a wineglassful of 
water for an adult. 

It. Antimonii et potassii tartratis, gr. ^; 

Codeiae, gr. —M. 

Ft. chart. No. j. 

Sig. One every two or three hours for an adult. 

The inhalation of menthol and compound tincture of 
benzoin is of great service. When the acute stage is passed 
astringent sprays may be employed. 

Attacks of dyspnoea in children are to be treated as are 
those of spasmodic laryngitis. 

CHRONIC CATARRHAL LARYNGITIS. 

Etiology. —This condition may result from repeated acute 
attacks, from breathing irritating dust or vapor, from excess- 


MEMBRA NO US LA R YNG1TIS. 


297 


ive smoking, and from over-use of the voice; it may com¬ 
plicate chronic bronchitis and pulmonary phthisis. The 
most common cause, however, is chronic nasal and pharyn¬ 
geal catarrh, especially if the nares be occluded and unfit for 
proper nose-breathing. 

Pathology.— Ihe mucous membrane of the larynx is 
congested and thickened, and the proper motility of the 
vocal cords is impaired. Secretion is excessive or scanty 
and tenacious. 

Symptoms.—There is a tickling, irritating cough, worse 
at night and in damp weather. The voice is husky, has no 
“ reaching power,” and may at times be lost entirely. Tick¬ 
ling sensations in the larynx cause a constant desire to clear 
the throat. 

Treatment.—The first thing is to remove the cause of the 
laryngitis, and especially to direct proper treatment to nasal 
and pharyngeal catarrhal conditions, should they exist. 
Heated rooms and impure air are to be avoided, smoking is 
to be prohibited, and proper exercise in the open air is to be 
insisted upon. Mufflers and neck-handkerchiefs should be 
avoided. Of great service are astringent sprays, especially 
nitrate of silver (gr. x : ,ij). Obstinate cases should be 
referred to a throat specialist. 

MEMBRANOUS LARYNGITIS. 

Etiology and Synonym.—The occurrence of a mem¬ 
branous laryngitis not diphtheritic in its nature is denied by 
some authors ; but cases undoubtedly occur in which the 
Klebs-Loeffler bacillus cannot be demonstrated, but in 
which streptococci and staphylococci play a causative role. 
Further bacterial examinations, however, are desirable to 
place these cases of non-diphtheritic membranous laryn¬ 
gitis upon a firm and independent basis. Synonym: Mem¬ 
branous croup. 


298 MANUAL OF THE PRACTICE OF MEDICINE. 

The pathology is practically that of diphtheria of the 
larynx, except that the deeper tissues are not, as a rule, so 
extensively infiltrated, and that the Klebs-Loeffler bacilli 
are not present. The exudation may be confined to the 
larynx, or it may spread to the trachea and bronchi, and 
more rarely to the pharynx, the palate, and the tonsils. 
In the exudate staphylococci and streptococci are found. 
The disease occurs in children between two and seven years 
of age almost exclusively. 

The symptoms of the non-diphtheritic laryngitis closely 
resemble those of the diphtheritic form, but they lack the 
extreme prostration so characteristic of diphtheritic toxaemia. 
The points of differential diagnosis from diphtheria are as 
follows: (1) The patient is a child between two and seven 
years of age ; (2) there is no history of exposure to diph¬ 
theria ; (3) the patient does not act as a source of contagion 
to others; (4) albumin and casts are not apt to be found in 
the urine; (5) the symptoms are those of laryngeal obstruc¬ 
tion and inflammation rather than those of obstruction, pros¬ 
tration, and sepsis ; (6) the lesion occurs in a primary form 
in the larynx, whereas in diphtheria the membrane on the 
larynx is almost invariably secondary to membrane on the 
pharynx, the tonsils, or the palate; (7) cardiac failure, 
peripheral neuritis with paralysis, and nephritis are not 
observed as sequelae. 

Treatment. —Owing to the necessary uncertainty of diag¬ 
nosis, the case should be isolated thoroughly from the start, 
and be considered as diphtheria. The treatment is that of 
laryngeal diphtheria in every particular, except that pharyn¬ 
geal irrigation need not be insisted upon. 

TUBERCULAR LARYNGITIS. 

Etiology and Synonym.—Tubercular infection of the 
larynx is almost always secondary to pulmonary tuber- 


TUBERCULAR LAR YNGIT 1 S. 


299 


culosis, in which it complicates from 18 to 30 per cent, of all 
cases. The larynx may be involved early or late in the 
course of the pulmonary disease. The occurrence of tuber¬ 
cular laryngitis is more common in men than in women, 
and between the twentieth and thirtieth years. Synonym: 
Laryngeal phthisis. 

Pathology. —The mucosa is thickened by tubercular 
deposits and by oedema, especially over the arytenoid car¬ 
tilages. Tubercles appear upon the surface, and often co¬ 
alesce to form masses, which may ulcerate. The resulting 
ulcers are broad and shallow, having grayish bases and 
being surrounded by thickened mucosa. There may be a 
destruction of the deeper tissues by extension of the ulcera¬ 
tion. The disease may spread to the pharynx, the epiglottis, 
or the oesophagus. 

Symptoms. —Hoarseness or aphonia constitutes an early 
and a constant symptom, to which, however, no diagnostic 



Fig. 22.—Tubercular laryngitis (Brown). 


importance can be attached, as the change of voice may be 
due to muscular insufficiency of the vocal cords or to 
chronic catarrhal laryngitis, to which conditions phthisical 
patients are extremely susceptible. There is usually an 
annoying painful cough, which is, however, sometimes 
absent even in aggravated cases. Pain on talking may be 
severe, and neuralgic pains running to the ears maybe com¬ 
plained of. Pain on swallowing may be so distressing that 












300 MANUAL OF THE PRACTICE OF MEDICINE. 

the patient is with difficulty prevailed upon to take suffi¬ 
cient food ; this pain usually results from tubercular involve¬ 
ment of the epiglottis or the pharynx. Dyspnoea may 
appear late in the disease, in either a constant or a parox¬ 
ysmal form, often necessitating tracheotomy to avert death 
from suffocation or to render the patient’s condition a trifle 
more endurable. 

The diagnosis is made by laryngoscopic examination. 
In the earlier stages of the disease the larynx is of a peculiar 
pallor, while the arytenoids show a characteristic club-like 
swelling Later in the disease the tubercular masses and 
ulcerations are easily recognized. A diagnosis is aided by 
finding tubercular changes in the lungs, and is rendered 
certain by the presence of tubercle bacilli in the secretion 
from the base of the ulcer. 

The prognosis for duration of life depends largely upon 
the primary pulmonary disease. Death may be hastened by 
suffocation, inanition, or exhaustion. 

Treatment is often unavailing. The larynx should be 
kept free of secretion by cleansing sprays. Astringents 
may be used by spray or insufflation, and powdered iodo¬ 
form may be insufflated with benefit. Pain in swallowing 
may be controlled by spraying the throat with a 2 per 
cent, solution of cocaine. Applications of lactic acid and 
submucous injections of creosote have been recommended 
warmly, but they should be used only by skilled specialists. 
P'or the relief of the dyspnoea tracheotomy may be indicated. 
Surgical treatment of tubercular laryngitis consists in the 
scraping out of tubercular deposits, the parts being exposed 
by a median thyroidectomy if necessary. 

SYPHILITIC LARYNGITIS. 

The hereditary form of syphilitic laryngitis usually appears 
in early childhood; it is characterized by the formation of 


(EDEMATOUS LARYNGITIS. 


301 

gummata, deep ulcerations, and cicatricial deformities. The 
acquired form is more common. 

As a secondary lesion the larynx may be the seat of an 
erythema, imparting to it a purplish-red, mottled appear¬ 
ance and giving rise to the symptoms of a simple laryngitis. 
Mucous patches and condylomata are rarely observed. 

As a tertiary lesion the disease is most common. There 
is a chronic catarrhal laryngitis, with an infiltration of the 
mucosa with gummata varying in size from a pin’s head to a 
hazelnut. These gummata may undergo resolution if the ap¬ 
propriate treatment be effectual, or they may ulcerate, fre¬ 
quently destroying the deeper structures. The lesions may 
involve the larynx or may be unilateral. Cicatrices follow the 
ulcerations, and they may be sufficiently extensive to cause 
great deformity. Laryngeal stenosis from such a cause is a 
frequent sequela. 

Treatment must be prompt and energetic—mercury for the 
secondary form, potassium iodide in large doses for the 
tertiary period, under the rules laid down for the treatment 
of syphilis. The larynx must be kept clear by sprays, and 
any resulting stenosis is to be treated by cutting or by dila¬ 
tation. Should the gummata be large enough to occlude 
the glottis, tracheotomy may be necessary to avert fatal 
dyspnoea. 


CEDEMATOUS LARYNGITIS. 

Etiology and Synonym. —CEdema of the glottis may 
complicate severe acute inflammation, whether due to cold, 
to inhalation of irritant vapors, or secondary to certain of 
the acute infectious diseases. It may occur with perichon¬ 
dritis, as in tubercular or syphilitic laryngitis, or it may be 
due to the spread of intense inflammations of neighboring 
parts. CEdema of the glottis may suddenly occur in the 
course of acute or chronic Bright’s disease, but this mode 


302 MANUAL OF THE PRACTICE OF MEDICINE. 

of occurrence is exceedingly rare. Synonym : (Edema of 
the glottis. 

Symptoms. —Dyspnoea is suddenly developed and be¬ 
comes rapidly urgent. The voice becomes husky and is 
finally lost. Respiration is accompanied by stridor. Symp¬ 
toms of asphyxia occur as a terminal event. 

The diagnosis can be made with certainty by laryngoscopic 
examination. The ary-epiglottidean folds are seen to be 
intensely cedematous, meeting in the median line in severe 
cases. The epiglottis may be involved by the oedema, and in 
rare cases the parts below the cords are also swollen. With¬ 
out the aid of the laryngoscope the diagnosis can usually 
be made by feeling the cedematous parts with the finger-tip. 

The prognosis is exceedingly bad. 

Treatment.—No time should be lost in temporizing. Ice 
poultices should be applied to the neck, and after spraying 
the throat with cocaine long incisions should be made into 
the cedematous parts with a curved bistoury protected ex¬ 
cept at the extreme tip. Tracheotomy should be resorted 
to unless prompt relief is afforded by the scarifications. 


2. DISEASES OF THE BRONCHI. 

ACUTE CATARRHAL BRONCHITIS. 

Etiology. —Primary bronchitis is exceedingly common 
as the result of “ catching cold,” beginning as a coryza and 
extending downward in the chest. It is more frequent in 
children and old people than in adults, and in the aged 
is a formidable disease. Cases are more common in the 
winter and spring months and in climates in which extreme 
and sudden changes in the weather occur. The disease is 
occasionally seen in localized epidemics, and it may even 
assume an apparently contagious nature. Those who lead 



ACUTE CATARRHAL BRONCHITIS. 


303 


an indoor life with insufficient ventilation are more suscep¬ 
tible, and those with “ delicate chests ” develop the disease 
upon the least provocation. It may be caused by the in¬ 
halation of noxious gases, such as ammonia, chlorine, or 
sulphurous acid, or by the breathing of smoke or of dust, 
especially in factories. 

Secondary bronchitis occurs with measles, influenza, 
whooping-cough, and any of the infectious diseases, and 
with diseases of the heart, lungs, or pleura. The considera¬ 
tion of these cases is referred to their respective headings. 

Pathology.— The lesion is bilateral, affecting the trachea 
and the larger and medium-sized bronchi. In severe cases, 
especially in children and old people, the smaller bronchi 
may be involved. The mucous membrane is congested, 
reddened, swollen, and covered with mucus and muco-pus 
containing desquamated epithelial cells and leucocytes. 
The mucous glands are enlarged. In severe cases the sub¬ 
mucosa is cedematous and is infiltrated with leucocytes. 

Symptoms.— In Adults .—There may be chilly feelings at 
the onset, followed by moderate fever, which rarely rises to 
103 0 F. even in the severest cases. Heaviness and malaise 
are present, with general pains in the bones, and the patient 
may be sick enough to be in bed. 

The chest symptoms set in with a feeling of tightness and 
oppression, a scraped feeling under the sternum, and a 
cough. At first the cough is dry, hoarse, and painful, com¬ 
ing in distressing paroxysms. Pain in the chest during 
coughing is chiefly felt along the attachments of the dia¬ 
phragm and down the sternum. When secretion is estab¬ 
lished the cough is much relieved. The sputum is at first 
scanty and mucous in character; it may be blood-streaked; 
later it becomes more abundant and muco-purulent. Dysp¬ 
noea is not a regular feature of bronchitis of adults, although 
in some patients there may be asthmatic breathing. 


304 MANUAL OF THE PRACTICE OF MEDICINE. 

Bronchitis in young children is a more serious disease, 
from its tendency to involve the smaller tubes and to merge 
into broncho-pneumonia. In young babies cough, fever, 
and rapid breathing may be the only symptoms. The rapid 
breathing makes it difficult to nurse these young infants. 
In older children the disease may be either mild or severe. 
In severe cases there may be convulsions at the outset. 
The fever is high (102° to 103° F.) with morning remis¬ 
sions ; the pulse is rapid ; the breathing is rapid and may be 
insufficient, as shown by duskiness of the skin and symptoms 
of carbon-dioxide poisoning. There is cough, but the sputa 
are regularly swallowed. There are apt to be gaseous dis¬ 
tention of the stomach and vomiting. It is often hard to 
tell where bronchitis ends and broncho-pneumonia begins. 
If the symptoms be severe, if they continue for three or four 
days without improvement, and if the physical signs point to 
the involvement of the smallest bronchi, it is best to regard 
the case as one of pneumonia. To this class of cases the 
term “ capillary bronchitis ” is given, but they are more 
properly cases of broncho-pneumonia. 

Bronchitis in old people is dangerous from the prostration 
and from the tendency of the disease to spread to the 
smaller tubes, and even to pass into broncho-pneumonia. 
There is a slight but irregular fever; prostration is extreme, 
the weakness interfering with the cough and the proper 
clearing out of the accumulated mucus. There is no com¬ 
plaint of dyspnoea, but the breathing is rapid and often is 
insufficient. There may be slight delirium, especially at 
night. 

Physical Signs.—The regular physical signs of bronchitis 
consist of coarse large and small mucous rales. In children 
bronchial fremitus is usually present. In the earlier stages 
there may be sibilant and sonorous breathing. Subcrepi¬ 
tant rales point to the involvement of the smaller tubes. 


ACUTE CATARRHAL BRONCHITIS. 


305 


Rales may be absent (1) in mild cases with scanty secretion, 

(2) in inflammation of the trachea and the large bronchi alone, 

(3) after coughing with the expulsion of the secretion, and 

(4) in the feeble and aged, in whom respiration is too feeble 
to generate rales. 

The prognosis is good except in young infants and in 
<>ld people, in whom broncho-pneumonia may develop. In 
the aged death from exhaustion may occur. 

The diagnosis of bronchitis is simple, but it is not to be 
considered complete unless it be determined whether the 
bronchitis is primary or is dependent upon some other 
disease, or whether it be an acute exacerbation of a chronic 
bronchitis. Bionchitis at an apex implies tubercular disease. 
Bronchitis of the finer tubes, worse at the apex and with 
continual high temperature, suggests miliary tuberculosis. 
Unilateral bronchitis suggests aneurysmal pressure, chronic 
interstitial pneumonia, or pleural adhesions. Bronchitis with 
dyspnoea and repeated slight hemorrhages suggests tuber¬ 
culosis or cardiac disease. Recurring attacks of bronchitis 
in young children suggest tuberculosis or tubercular bron¬ 
chial glands. 

Treatment.—In the majority of cases no treatment is re¬ 
quired. Much can be done to abort an attack by free dia¬ 
phoresis at the onset. A Dover’s powder at night with a hot 
mustard foot-bath often suffices. A hot lemonade contain¬ 
ing a little whiskey is a popular and efficacious remedy. 
Turkish baths are objectionable from the danger of catch¬ 
ing more cold on leaving the bath-house, but a hot bath at 
night is often useful if the patient need not leave the house 
afterward. The bowels should be opened by salines, and 10 
grains of quinine in a single dose may be given. Delicate 
patients should be kept indoors or in bed. Expectorants 
are very useful to promote free secretion, but they are often 
given indiscriminately. They may be combined with seda- 
20 


306 manual of the practice of medicine. 

tives. In the dry stage tartar emetic in gr. ^ doses every 
two hours until slight nausea is experienced is often service¬ 
able, but preparations of squills, senega, ipecac, or ammo¬ 
nium muriate may be used. The sedatives employed are 
codeia and dilute hydrocyanic acid or small doses of opium. 
The following formula is recommended : 


Codeiae, 

g r - i; 

Ammon, muriat., 

gr- ij ; 

Acid, hydrocyanic, dilut, 

, miij; 

Syrup, scillae comp., 

mx; 

Infus. prun. Virg., 

ad 3j.—M 


Sig. Dose every two or three hours for an adult. 

When free secretion is established, ammonium muriate with 
mist, glycyrrhizae comp, is of much benefit. The paroxysmal 
cough of the earlier stages is frequently benefited by the 
inhalation of steam, to which maybe added compound tinc¬ 
ture of benzoin or terebene. If the disease threaten to 
become chronic, the patient should be put upon a support¬ 
ing tonic treatment, and, if possible, be sent away to some 
warm, dry, inland place. 

Bronchitis in children is to be treated like that in adults, 
except that opiates are not well borne. Severe cases are to 
be treated like broncho-pneumonia. If the bronchi become 
blocked by a too profuse secretion, interfering with free 
respiration, a simple emetic should be given. Bronchitis in 
old people frequently requires stimulation by alcohol, digi¬ 
talis, and strychnine. Opiates are to be used with extreme 
caution. 


ACUTE CROUPOUS BRONCHITIS. 

Etiology and Synonyms. —The disease is rare. It may 
occur as the result of breathing irritating vapors and steam, 
but it is more often secondary to diphtheritic or croupous 


ACUTE CROUPOUS BRONCHITIS. 


307 

laryngitis by extension downward. Synonyms: Acute 
fibiinous bronchitis; Acute membranous bronchitis; Diph¬ 
theritic bronchitis. 

The lesion is that of a croupous inflammation of a mu¬ 
cous membrane. In cases complicating laryngeal diphtheria 
the Klebs-Loeffler bacilli are present in the membrane. 

Symptoms. There may be a chill with fever and pros¬ 
tration at the onset, or there may be the previous history 
of membranous laryngitis. When developed, there is a 
cough with muco-purulent expectoration. From time to 
time there will be attacks of paroxysmal cough with the 
expectoration of rolled-up casts of a bronchus and its 
branches. These casts consist chiefly of coagulated fibrin 
which in places has undergone hyaline degeneration, and in 
its meshes are leucocytes, epithelial cells, and frequently Ley¬ 
den’s crystals and Curschmann’s spirals. These casts readily 
unroll in the water. During the coughing attack suffoca¬ 
tion seems imminent, and often some blood is raised, but 
after the cast is expectorated the distress abates. Between 
the coughing attacks the symptoms resemble severe acute 
bronchitis, frequently with symptoms of insufficient aeration 
of the blood and of dyspnoea. 

The physical signs consist of bronchial rales of all kinds, 
fine and coarse, with sibilant and sonorous breathing - 
When a bronchus is occluded, breathing sounds may be 
absent over that portion of lung, returning, however, when 
the occluding membrane is coughed up. 

The prognosis is bad, depending on the nature of the 
primary disease and the extent of the bronchi involved. 
Death usually occurs from suffocation. It is a most serious 
complication after tracheotomy. 

The treatment is that of acute bronchitis, except that 
inhalation of steam is often of service in loosening the false 
membrane. For this purpose hypodermics of pilocarpine 


308 manual of the practice of medicine. 

may also be employed. Inhalations of pure oxygen gas are 
of benefit if symptoms of asphyxia appear. 

CHRONIC CATARRHAL BRONCHITIS. 

Etiology.—Chronic catarrhal bronchitis may occur after 
repeated acute attacks, but it is not common except in rheu¬ 
matic and gouty patients. It is most commonly secondary 
to emphysema, to any chronic inflammation of the lung, to 
pleural adhesions, and to organic heart disease. It usually 
occurs in elderly people; it is more common in the winter 
months. 

Pathology.—The mucous membrane of the bronchi may 
be thinned, and the muscular and glandular coats may be 
either atrophied or thickened and granular. There may be 
superficial ulcerations. Bronchial dilatation is not uncom¬ 
mon. Emphysema is usually present. 

The symptoms persist for years—better in summer, worse 
in winter. There is a cough which is worse at night. The 
expectoration varies greatly. In some cases it is scanty— 
the so-called “ dry catarrh/’ an obstinate form with severe 
and paroxysmal cough. The term “ bronchorrhoea ” is ap¬ 
plied to cases with excessive secretion. The expectoration 
may be thick and yellowish or greenish, or more watery in 
character, depending upon the relative proportions of pus, 
mucus, and serum. If bronchiectatic cavities are present, 
the patient will often raise large quantities of secretion by 
any change of position which allows the cavity to drain 
itself. Dyspnoea is not marked except from associated em¬ 
physema or cardiac disease, although some patients develop 
asthmatic breathing from time to time. There may be mild 
constitutional symptoms, especially during the winter 
months—emaciation, slight afternoon rise of temperature, 
and loss of strength. 

Fetid bronchitis occurs when the secretions decompose, 


CHRONIC CATARRHAL BRONCHITIS. 


309 


especially in bronchiectatic cavities, in tubercular cavities, 
with abscess and gangrene of the lung, and in empyema 
with a pulmonary fistula. 

Fetid expectoration may occur in chronic bronchitis; it 
is likely to lead to bronchiectasis, pneumonia, or gangrene 
of the lung. In these cases it is often difficult to say which 
is the primary disease. 

The physical signs are those of bronchitis—coarse and 
subcrepitant rales, with sibilant and sonorous breathing. 
Bronchiectatic cavities yield their regular physical signs. 
If the bronchitis be secondary to pulmonary or cardiac dis¬ 
ease, the physical signs of such disease are present. 

The prognosis is bad for complete recovery, although 
patients live for years in comparative comfort. 

Treatment.—The best possible treatment is to send the 
patient for the winter to some warm, equable climate. In 
every case the primary disease should be treated, gouty and 
rheumatic habits corrected, the bowels regulated, the diet 
supervised, and every attention paid to the general nutrition. 
The ordinary expectorants are not of much service. Iodide 
of potassium in 5- or 10-grain doses three times a day often 
has a certain curative influence; it should always be tried. 
Ammonium chloride in 10- or 15-grain doses every two or 
three hours does good when the secretion is abundant. If 
there be profuse purulent secretion, turpentine, terpin and 
terpin hydrate, cubebs, and oil of sandalwood should be 
tried. For distressing cough the syrup of tar, with or with¬ 
out the syrup of wild cherry or the fluid extract of chekan, 
may be used. The latter is to be given in 3j doses every 
three hours, and the most desirable way of administering it 
is to evaporate it to a solid extract, which can be given in 
capsule, after the common method of administering War¬ 
burg’s tincture. 

If fetid bronchitis occurs, myrtol may be used in 2- to 


310 MANUAL OF THE PRACTICE OF MEDICINE. 


5-grain doses three times a day. Oil of sandalwood and 
terpin hydrate are also of service, while the odor may be 
lessened by means of sprays of carbolic acid or of thymol. 

CHRONIC CROUPOUS BRONCHITIS. 

Etiology and Synonyms.—Nothing definite is known 
about this rare disease, except that it is more common in 

adults and in males, and that it 
is often associated with phthisis. 
Synonyms: Membranous bron¬ 
chitis ; Fibrinous bronchitis; 
Plastic bronchitis. 

The symptoms of chronic 
bronchitis are present, and from 
time to time the patient has a 
severe coughing attack, possibly 
with spitting of blood, and raises 
a cast of a bronchus and its 
branches. These casts consist 
of an unknown albuminoid sub¬ 
stance, probably of altered fibrin. The attacks occur at 
varying intervals extending over years, as the disease is 
essentially chronic. 

The prognosis for life is good ; for recovery from the 
bronchitis, bad. 

The treatment is that of chronic bronchitis. 

BRONCHIECTASIS. 

Definition.—Bronchietasis is a dilatation of the bronchial 
tubes. 

Etiology.—The disease is always secondary to some 
lesion weaking the bronchial wall, so that it dilates under 
coughing pressure. 



Fig. 23.—Fibrinous bronchial cast. 




BRO NCHIE C TA S/S. 


3 11 

1. There may be congenital weakness of the bronchial 
wall, usually unilateral, but these cases are extremely rare. 

2. Inflammation of the bronchial wall leading to atrophic 
changes in the muscular and fibrous structures is the opera¬ 
tive cause in the large majority of cases; hence the disease 
occurs with chronic bronchitis, emphysema, broncho-pneu¬ 
monia of children, phthisis, foreign bodies within the 
bronchi, or pressure from an aneurysm or a tumor. 

3. The bronchial wall may be weakened by traction from 
without, from old pleuritic adhesions, interstitial pneumonia, 
and fibroid phthisis. 

Pathology.—A cylindrical and a sacculated form of bron¬ 
chiectasis are recognized. The two forms may coexist in 
the same lung. The dilatation varies in size from a pea to 
that of a small orange. Sacculated dilatations are usually 
multiple, being spread along the course of a bronchus. 
A single sacculated bronchiectasis surrounded by non- 
indurated lung-tissue may occur with emphysema and 
bronchitis in rare instances, and may resemble a single 
cyst without contents. The bronchial wall is thinned and 
its constituent elements are atrophied. The mucous mem¬ 
brane constituting the lining of the cavity may be normal or 
smooth and glistening, the columnar having been replaced 
by pavement epithelium, or it may be infiltrated and thick¬ 
ened, or it may be extensively ulcerated, especially in cases 
where the secretions are retained. The contents of some 
of the larger cavities are often exceedingly fetid, and a 
general fetid bronchitis may complicate the disease. 

Symptoms.—Moderate bronchiectasis does not, as a 
rule, give rise to symptoms or physical signs, and it cannot 
be recognized during life. The larger dilatations are diag¬ 
nosed by the cough and the expectoration. After a period 
of some hours free from cough a paroxysm will occur, dur¬ 
ing which large quantities of sputum are raised, frequently 


312 MANUAL OF THE PRACTICE OF MEDICINE . 


“by mouthfuls.” These coughing attacks usually occur in 
the morning upon arising; they may be brought on by 
any position of the body that allows the secretion to flow 
from the dilatation into a normal tube. The sputum is 
abundant, frequently is foul-smelling, and separates on 
standing into three layers—the upper of a brownish froth, 
the middle of watery mucoid substance, and the lowest of 
a thick sediment of granular matter and cells. When ulcera¬ 
tion occurs there may be present haematoidin-crystals and 
elastic fibres. Hemorrhage may occur, but it is rare. 

The physical signs are not pronounced except in the 
well-marked cases. Large saccular “ dilatations” give rise to 
the physical signs of cavities, associated with the evidences 
of the disease to which the bronchiectasis is secondary. 
The caverous signs vary from time to time according to the 
amount of accumulated secretion; these signs are often 
localized at the base of the lung—a point of considerable 
importance in the diagnosis between this lesion and a tuber¬ 
cular cavity. The physical signs may closely resemble a 
sacculated empyema with an opening into a bronchus, but 
the history of the case will usually make the diagnosis evi¬ 
dent. 

Prognosis.— The condition is essentially chronic, often 
lasting for years, during which time the patient may enjoy 
an active life. The prognosis is rendered worse by the 
primary lung conditions, by hypertrophy and dilatation of 
the right ventricle secondary to interstitial pneumonia, and 
by the possibility of an added tubercular infection or of 
pulmonary gangrene. 

Treatment is unsatisfactory, because it is inadequate to 
heal the dilatation. The cough is beneficial in clearing 
out the accumulated secretions, hence narcotics are inadmis¬ 
sible. Stimulant expectorants are useless. Some benefit 
may result from the administration of terpin hydrate in full 


ASTHMA. 


313 


doses, terebene, and turpentine. Injection of antiseptic solu¬ 
tions into the cavities has been followed by good results in 
some cases. In patients in good condition, with superficial 
cavities, incision and drainage may be resorted to. For the 
fever myrtol may be given internally, and inhalation of car¬ 
bolic acid (1 to 3 per cent, solution) and of thymol (1 : 1000), 
as described under Fetid Bronchitis; the results, however, 
are never very satisfactory in extreme cases. 

ASTHMA. 

Definition.—Asthma is an affection characterized by 
paroxysmal dyspnoea due to contraction of the bronchi. 
I he same name also designates the paroxysmal dyspnoea, 
due to the contraction of the arteries, commonly seen with 
emphysema. 

Etiology.—A number of theories have been advanced to 
explain the symptoms : (1) That the disease is due to spasm 
of the muscular tissue of the small bronchi (Biermer). (2) 
That it is due to spasm of the diaphragm and the accessory 
muscles of respiration (Wintrich-Bamberger). (3) That it 
is a vaso-motor neurosis causing sudden swelling of the 
bronchial mucous membrane (Storck, Sir Andrew Clark, 
Traube). (4) That it is due to the elimination of Leyden’s 
crystals. (5) That it is a special form of inflammation of 
the bronchioles—bronchiolitis exudativa (Curschmann). Of 
these theories, the first, that of bronchial spasm, is the one 
generally adopted. 

The causes of the disease are both predisposing and 
exciting. 

Predisposing Causes .—The disease is more common in 
those with high-strung nervous systems ; it may run in 
neurotic families associated with epilepsy or with neuralgia. 
Males are more frequently affected than females. As to 
age, of 225 cases, 71 occurred in the first decade, 30 in the 


314 MANUAL OF THE PRACTICE OF MEDICINE. 

second, 39 in the third, 44 in the fourth, 24 in the fifth, 12 
in the sixth, 4 in the seventh, and I in the eighth. The 
predisposition to the disease is frequently retained through¬ 
out life. The affection is more common in those with pul¬ 
monary emphysema. 

Exciting Causes .—Climatic influences are very curious, 
some patients having asthma in some places and not in 
others, without apparent reason. Vegetable and terrestrial 
dust and irritating vapors may induce an attack. In this 
respect asthma closely resembles hay fever, with which dis¬ 
ease it is closely allied, and which it frequently complicates. 
Ipecac, sulphur, iodine, the pollen of many flowers and 
grasses, the irritant odor of violets, roses, and strawberries, 
the dust of feathers, and the emanations of certain animals 
afford familiar examples of personal susceptibility. Sudden 
mental shocks and deep emotions may induce asthma. The 
most frequent cause of an attack in those predisposed to 
asthma is bronchitis, and if in such patients bronchitis can 
be avoided, attacks of asthma are rare. 

Reflex causes are common. Nasal polypi, hypertrophic 
rhinitis, naso-pharyngeal adenoids, and enlarged tonsils are 
frequently found, and the cure of these conditions will in 
many cases remove the liability to asthma. It is too much 
to claim that nasal and pharyngeal lesions comprise the 
only cause, however, as has been done by some. Among 
other reflex causes are uterine and ovarian diseases, over¬ 
loading of the stomach, and the taking of certain articles 
of food. 

Pathology.—As asthma is a functional disease, there is no 
regular lesion, although in old asthmatics emphysema and 
chronic bronchitis are often present. 

Symptoms.—There may be premonitions—a sense of 
drowsiness, depression of the mind, tightness in the chest, 
or peculiar feelings in individual cases that mean an impend- 


ASTHMA. 


315 


ing attack. The paroxysm usually begins at night with a 
sense of dyspnoea and with laborious efforts at breathing. 
The patient cannot lie down, but sits or stands, usually by 
an open window. Inspiration is spasmodic; expiration is 
prolonged and wheezing. The accessory muscles of respi¬ 
ration are called into play; the face is livid and distressed, 
and perhaps cyanotic. Limpid urine is usually passed in 
large quantities. There is a cough, tight at first, with ball¬ 
like gelatinous masses of sputum—the “ perles” of Laennec. 
These balls can be unrolled in water; they represent mucous 
casts of the smaller bronchi. They frequently have a dis¬ 
tinct spiral form, and they are known as “ Curschmann’s 
spirals ” (Fig. 24), in which there is frequently a central 



Fig. 24. —Curschmann's spirals : a, central fibre (after Curschmann). 


translucent filament composed of altered mucin. In addi¬ 
tion are found in the sputum the pointed octahedral crystals 
described by Leyden, identical with those found in semen 
and in leukaemic blood (Fig. 25). 

Physical Signs.—The chest is fixed and enlarged—often 
from 6 to 8 centimeters larger in circumference than nor¬ 
mal. Expansion is poor, especially laterally, and is in 
strong contrast to the muscular attempts of respiration. 
Inspiration is short; expiration is prolonged and wheezing. 


316 MANUAL OF THE PRACTICE OF MEDICINE . 


The diaphragm is low and moves but slightly. Percussion 
shows an increased area of pulmonary resonance. The 
note may be normal or hyper-resonant or tympanitic. On 
auscultation are heard all varieties of sibilant, sonorous, 
cooing, and whistling rales, especially during expiration. 



Fig. 25. —Charcot-Leyden’s asthma-crystals (after Riegel). 


The expiratory murmur may be prolonged, or breathing 
sounds may be absent or be obscured by the rales. 

The duration of the attack varies from several hours to a 
number of days. In the more protracted cases the symp¬ 
toms are worse at night. Between the attacks there may 
be dyspnoea, wheezing respiration, and cough. In the long¬ 
standing cases emphysema and chronic bronchitis develop, 
resulting in chronic invalidism. 

The prognosis for life is good, death never resulting dur¬ 
ing a paroxysm. 

Treatment .—During the attack immediate treatment is 
required to relax the contracted bronchioles. A number of 









ASTHMA . 


317 


remedies may be employed, Of these remedies amyl nitrite 
is the most serviceable, a perle containing from 2 to 5 minims 
being broken in a handkerchief and the vapor inhaled. Hot 
stimulants or spirits of chloroform in hot water may be 
given, while whiffs of chloroform may be required in aggra¬ 
vated cases. Permanent relief is often afforded, even in 
obstinate cases, by a hypodermic injection of morphine. 
Nitroglycerin, gr. every two or three hours, is of service 
in the more protracted cases. Choral in 10- or 15-grain 
doses often affords relief. Antipyrine, gr. xv, or phenacetine, 
gr. x, may be used, repeated every three hours. Good 
results are claimed for the fluid extract of grindelia robusta 
in 3j doses every four hours. The smoke of cigarettes 
containing hyoscyamus, belladonna, or stramonium may be 
inhaled, or pastilles may be made from these drugs, with 
the addition of potassium chlorate or nitrate. Inhalations 
of cigar-smoke are frequently of great value. Paper satu¬ 
rated with a strong solution of potassium nitrate burnt 
in the room before retiring will often ward off a nocturnal 
attack. 

Between attacks antispasmodics should be given. Iodide 
of potassium in gr. v-xv doses three times a day, with or 
without the addition of 5 grains of chloral to each dose, is 
of great benefit. Nitroglycerin, gr. every four to six 
hours, may be used. The systematic inhalation of com¬ 
pressed air has been recommended strongly. 

The diet should be such as not to induce flatulence, 
carbohydrates being used in great moderation. The patient 
should not retire to bed on a full stomach, and it is usually 
best for the heavy meal of the day to be taken at noon. 

If nasal polypi or hypertrophies are present, they should 

be removed. 

For every asthmatic there are localities in which he has 
little or no asthma. The particular locality of exemption 


31 8 MANUAL OF THE PRACTICE OF MEDICINE. 


should be found by each patient to suit his individual case, 
as no regular rule can be laid down to suit all patients. 


3. DISEASES OF THE LUNGS. 

(a) Circulatory Disturbances. 

CONGESTION OF THE LUNGS. 

Congestion may be either active or passive. 

Active congestion occurs with acute inflammation of the 
lungs, with over-action of the heart, and from the inhalation 
of hot or irritating vapors. It may cause increase of dysp¬ 
noea, cough, and expectoration, with a moderate degree of 
fever, but about its symptomatology not much is accurately 
known. 

Most authors describe a rapidly fatal form of congestion 
occurring after exposure to cold or after over-exertion. 

Passive Cojigestion. —Two distinct forms of passive con¬ 
gestion are recognized—mechanical and hypostatic. 

1. Mechanical congestion is known as “ brown induration ” 
or the “ pneumonia of heart disease ” ; it is described under 
the heading of Chronic Venous Congestions of Heart 
Disease, page 209. 

2. Hypostatic congestion of the posterior portions of the 
lungs is often found as the result of post-mortem changes. 
It is common in those confined to bed for a long time in a 
weakly condition, as the combined result of feeble circula¬ 
tion and the effect of gravity. In coma and in cerebral 
injuries, such as cerebral hemorrhage, it is often seen in its 
most pronounced degree. The affected portions of lung are 
congested, oedematous, heavy, and imperfectly aerated. 

The congestion may be complicated by patches of con¬ 
solidation resembling either broncho-pneumonia or a lobar 



(EDEMA OF THE LUNGS. 


319 

pneumonia, being due to the passage into the bronchi of 
food or air containing streptococci. 

The symptoms are usually obscured by those of the 
primary disease, so that a diagnosis is to be made by phys¬ 
ical signs. There is dulness over the congested portions, 
with feeble breathing and liquid rales. In more advanced 
cases there may be bronchial breathing and bronchophony. 

CE3DEMA OP THE LUNGS. 

Localized oedema of the lungs occurs with congestion, 
inflammation, and new growths; it is known as “ collateral 
oedema.” 

General pulmonary oedema occurs from weakness of the 
left side of the heart, the force of the right heart being 
unimpaired, or it may occur in pronounced conditions of 
hydraemia. Either cause alone may suffice for its produc¬ 
tion, although in extreme cases both factors are usually 
present. It is often present during the death agony, being 
a symptom of approaching death. It is seen in the final 
stages of cachexias, profound anaemia, acute and chronic 
Bright’s disease, pneumonia, cerebral diseases, and diseases 
of the heart. 

The lungs are heavy, pit on pressure, and from their cut 
section exudes a frothy serous or sero-sanguinolent fluid in 
abundance. This fluid is also present in the trachea and 
the bronchi. The oedema interferes with the proper degree 
of aeration, although cut pieces of the lung still float in water. 
There is usually associated congestion of the lungs, espe¬ 
cially of the posterior portions. 

The symptoms are increasing frequency of respirations, 
dyspnoea with cough, and the expectoration of serum which 
may be blood-tinged. The respirations are bubbling and 
rattling, and cyanosis, increasing coma, and cold, clammy 
extremities precede the fatal issue. The percussion-note 


320 MANUAL OF THE PRACTICE OF MEDICINE. 

over the oedematous portions is more or less dull; the respi¬ 
ratory murmur is feeble or is obscured by large liquid rales 
and bubbling sounds usually first heard at the bases. 

The treatment is that of the primary condition. The heart 
should be stimulated energetically; cups and poultices are 
to be applied to the chest, and the bowels should be moved 
freely. Venesection should be resorted to in acute cases 
with cyanosis; it frequently affords relief. 

PULMONARY HEMORRHAGE. 

Two forms of pulmonary hemorrhage are recognized: 
I. Broncho-pulmonarv hemorrhage, or bronchorrhagia, in 
which condition the blood is poured into the bronchi and 
is expectorated ; 2. Pulmonary apoplexy, or pneumorrhagia, 
in which disease the hemorrhage occurs into the substance 
of the lung. 

Broncho-Pulmonary Hemorrhage, or Hemoptysis. 

There is a variety of causes giving rise to this condition. 

(a) Pulmonary tuberculosis is the most common cause, 
and it should always be suspected, even if neither symptoms 
nor physical signs be present. Small repeated hemorrhages 
in the earlier stages are due to bronchial congestion or 
ulceration. Large hemorrhages in the later stages arise in 
cavities from erosion of a branch of the pulmonary artery 
or from rupture of an aneurysmal dilatation of the same. 

(/;) Hemorrhages may occur in young people without 
assignable cause, although in some cases they may follow 
excitement or severe muscular exertion, especially in high 
altitudes. 

(<:) Anaemic hysterical women may raise a little blood 
from time to time without apparent reason. Deception 
must always be suspected in such cases, however. 


PULMONARY HEMORRHAGE. 32 1 

( d) Severe injuries and contusions of the chest are often 
followed by hemorrhage. 

(e) Patients with emphysema and bronchitis may occa¬ 
sionally raise small quantities of blood. 

(f) Hemorrhage may result from certain diseases of the 
lung, the initial stage of pneumonia, cancer, gangrene, 
abscess, or bronchiectatic cavities. 

(g) Vicarious haemoptysis may occur with interrupted 
menstruation. It has been known to follow removal of 
both ovaries. 

(h) Small repeated hemorrhages are common with the 
pulmonary congestion of heart disease, especially with 
lesions of the mitral valve. 

(1) With aneurysms small quantities of blood may be raised 
from congestion of the bronchi from pressure or by leakage 
through a small perforation. Large and fatal hemorrhage 
results from rupture of the sac into the trachea or into a 
bronchus. 

(j ) Any ulcerative process in the larynx, the trachea, or 
the bronchus may cause small repeated hemorrhages. 

(k) Sir Andrew Clark describes a form of haemoptysis, 
seen in elderly people, which he calls “ arthritic haemop¬ 
tysis.” It occurs in those of the arthritic diathesis; it is 
due to minute structural alterations in the terminal blood¬ 
vessels of the lung. The prognosis in these cases is usually 
good. 

(/) Haemoptysis occurs with extensive blood-alterations 
of malignant fevers, as hemorrhagic variola, and with pur¬ 
pura haemorrhagica. 

(in) In Japan and China occurs an endemic haemoptysis 
due to the presence of the Distoina Ringeri in the bronchi. 

Symptoms.—There may be a preceding feeling of oppres¬ 
sion in the chest, but usually the first symptoms are a warm, 
mawkish taste in the mouth, nausea and faintness, and the 
21 


322 MANUAL OF THE PRACTICE OF MEDICINE. 

appearance of the blood. The quantity of blood ejected 
varies from a dram to a pint or more. 

Anaemic symptoms—faintness, syncope, dyspnoea, “ air- 
hunger,” and pallor—depend on the quantity of blood lost. 
Large hemorrhages mav be fatal from anaemia or from the 
filling of the bronchi with blood, but usually danger is 
not imminent. There is generally but little effort in raising 
the blood. Should the quantity be large, a certain amount 
may be swallowed, to be vomited later or passed with the 
stools. Blood from the lungs has certain characteristics 
which distinguish it from blood from the stomach. It is 
scarlet in color, of an alkaline reaction, frothy, and mixed 
with mucus. In the clots air-bubbles can usually be seen. 
After a hemorrhage the sputa are usually blood-stained, of 
a dark crimson or brown color, and frequently clots like 
bronchial casts are raised. Vomited blood is dark brown¬ 
ish, contains no air, but is mixed with stomach-contents 
and is of an acid reaction. Blood coming from the pharynx 
or the nares is usually hawked up, and on inspection blood- 
streaks can almost always be seen descending from the 
naso-pharynx. 

Large hemorrhages, leading even to a fatal issue, can 
take place into extensive pulmonary cavities without blood 
being coughed up at all. The hemorrhage may continue 
for several hours or even days, and attacks may be repeated 
from time to time. They may be induced by exertion, by 
over-indulgence in stimulants, or by excitement, but in 
some cases they occur without apparent cause, even while 
the patient is resting quietly at night. 

Anaemic symptoms follow large hemorrhages, but after 
small hemoptyses the patients frequently feel much relieved 
in their pulmonary or cardiac symptoms. 

Treatment. —For the large hemorrhages arising from 
erosion of an artery or from rupture of an aneurysm treat- 


PULMONARY HEMORRHAGE. 


323 


ment is unavailing. The patient should be kept absolutely 
quiet and secluded, and small doses of opium should be 
given to relieve the restlessness and steady the heart. 
Fainting is nature’s measure of tranquillizing the circulation 
and inducing firm thrombosis. 

Anaemic symptoms are treated by elevation of the foot 
of the bed, by ligating the extremities, and by hypodermic 
injections (hypodermoclysis) or arterial transfusion of ster¬ 
ilized saline solutions, which may also be given by the 
rectum. Internal haemostatics are useless. 

In less serious hemorrhages the patient may be given ice 
to swallow and may drink small quantities of aromatic sul¬ 
phuric acid in water. Theoretically, measures to reduce the 
frequency of the heart-beats and reduce the blood-pressure 
in the pulmonary circulation are indicated, but our know¬ 
ledge as to how this latter indication can be fulfilled is very 
meagre. Rest should be enforced, and opium be given to 
quiet the patient. The diet should be light, and stimulants 
should not be employed. Digitalis is contraindicated. Aco¬ 
nite may be given with benefit if there be vascular excite¬ 
ment. Acid drinks and cracked ice may be given. Ergot, 
gallic acid, acetate of lead, hydrastis, and krameria are used 
as routine measures, but are of doubtful utility. Ice applied 
to the chest is recommended, and in some cases it seems 
to do good. Free purgation is indicated to reduce blood- 
pressure ; it should be resorted to in all protracted cases. 

Pulmonary Apoplexy ; Hemorrhagic Infarct. 

Hemorrhage into the substance of the lung, with rupture 
of its tissue, may occur with severe contusions, with pene¬ 
trating wounds, and with rupture of an aneurysm. Aside 
from these cases, so-called “ hemorrhagic infarcts ” result 
from embolism or thombosis of a branch of the pulmonary 
artery, resulting in the stoppage of its circulation. As these 


324 MANUAL OF THE PRACTICE OF MEDICINE. 

are “ terminal ” arteries, without anastomotic branches, the 
blood in the vessels beyond the obstruction is in a condition 
of stasis, and congestion occurs from a backward pressure 
into the shut-off region. The vascular walls lose their con¬ 
sistency and allow the escape of blood into the surrounding 
structures. 

The hemorrhagic area is red and solid, resembling a blood- 
clot, becoming reddish-brown in time from pigment-changes. 
It is of a wedge shape with the base out; the pleura covering 
it is usually inflamed. It is usually situated toward the base, 
and it varies in size from a walnut to that of an orange. 
There may be a surrounding zone of pneumonia. Such an 
infarction may be absorbed if small, but it usually becomes 
changed to a pigmented, puckered cicatrix. In rarer cases 
it may undergo sloughing or gangrene. Abscess results if 
the cause be an infectious embolus containing suppurative 
micrococci, as may occur in pyaemia or in malignant endo¬ 
carditis. 

Symptoms. —There is usually pain in the side, sudden 
dyspnoea, oppression in the chest, and bloody expectora¬ 
tion, in some cases amounting to a fair-sized haemoptysis. 
Physical examination yields over the hemorrhagic area, if it 
be of sufficient size, dulness, bronchial voice and breathing, 
and pleuritic and bronchial rales. Large hemorrhagic in¬ 
farcts may be followed by sudden death. It must be remem¬ 
bered that obstruction of a large branch of the pulmonary 
artery can occur without the formation of a hemorrhagic 
infarct. 

The treatment is practically that of pneumonia. 

LOBAR PNEUMONIA. 

Definition and Synonyms.—Lobar pneumonia is an in¬ 
fectious disease due to the diplococcus pneumoniae; it is 
characterized by an inflammation of the lung with consti- 


LOBAR PNEUMONIA. 


325 

tutional symptoms. Synonyms: Croupous or Fibrinous 
Pneumonia; Pneumonitis. 

Etiology.—The diplococcus pneumoniae of Frankel, 
commonly known as the “ pneumococcus/' is the specific 
geim of the disease. It is an ovoid coccus, or, more prop¬ 
erly speaking, a bacillus, usually occurring in pairs, and more 
often encapsulated. It is found in the nasal and buccal 
secretions of 20 per cent, of healthy people, and after an 
attack ot pneumonia it is often found in the mouth for 
months ; hence there must be conditions giving the germ at 
times more intense pathogenic properties, or conditions ren- 



Fig. 26. Frankel’s pneumonia coccus, bred from the expectoration. (Prepared by Prof. 

Gartner. Oil-immersion lens fa; eye-piece No. 4.) 

dering the individual susceptible to the infection. Among 
these causes may be mentioned exposure to hardship and 
cold; consequently the disease is more frequent in men 
than in women. It frequently follows immersion in cold 
water. Traumatisms of the chest-wall produce the so-called 
“ contusion-pneumonia.” Alcoholism, chronic Brio-ht’s 
disease, and any condition of bodily weakness predispose 
to the disease. Repeated attacks may occur ; they are ex¬ 
plained by auto-infection from the persistence of diplococci 
in the buccal and nasal secretions. The disease is more 
common in the months from February to May, although it 
may occur at any time. It occurs in all temperate climates, 
but it is unknown north of Labrador. It is more frequent in 






326 MANUAL OF THE PRACTICE OF MEDICINE. 

the Southern than in the Northern States. The influence of 
age is important. Liability to the disease increases up to 
the twentieth year, then decreases until liability is again 
increased in old age. Children under five years of age 
usually have broncho-pneumonia; those between five and 
fifteen years of age have either lobar pneumonia or broncho¬ 
pneumonia ; adults usually have lobar pneumonia. 

The diplococci are found not only in the exudate in the 
inflamed lung, but also in many of the complicating lesions, 
as in the meninges, the pleura, or the pericardium ; they may 
even involve these parts without there being any inflamma¬ 
tion of the lung at all. 

Pathology. —The lesion involves a whole lobe, a part of 
a lobe, or the entire lung. The lower lobes are more 
frequently involved than the upper; the right lung is more 
often involved than the left. The process is divided into 
four stages : congestion, red hepatization, gray hepatization, 
and resolution. 

Congestion .—The lung is congested and heavy; its cut 
surface is bathed with bloody serum. Microscopic exami¬ 
nation shows congestion of the blood-vessels and swelling 
and proliferation of the alveolar epithelium, while the air- 
cells are partially filled by an exudate of fibrin pus-cells, 
red blood-corpuscles, and epithelial cells. The stage of 
congestion usually lasts for several hours, but it may be 
protracted for several days. 

Red Hepatization .—The lung is large, often showing in¬ 
dentations of the ribs, and is remarkably friable. It is hard 
and airless, cut pieces sinking in water. There is fibrin on the 
pulmonary pleura. The cut surface is dry, reddish, and dis¬ 
tinctly granular, due to the protrusion of inflammatory exu¬ 
date from the air-cells. The microscope shows the air-cells, 
and frequently the small bronchi as well, filled with an exu¬ 
date of fibrin, pus-cells, red blood-cells, and epithelium. 


LOBAR PNEUMONIA. 


327 


The blood-vessels are congested but pervious. The inter¬ 
stitial connective tissue of the lung may be infiltrated with 
inflammatory exudate. Diplococci, and occasionally staph¬ 
ylococci and streptococci as well, are seen in the exudate. 
One-fourth of the fatal cases occur in red hepatization from 
the first to the eleventh day of the disease. 

Gray Hepatization .—The color changes from reddish- 
brown to gray, at first in spots, so that the lung has a mot¬ 
tled appearance. The lung still remains solid, but the 
exudate is decolorized and begins to soften and degenerate. 
One-half the fatal cases occur in the mottled condition, 
between the second and the eighteenth day, and one-fourth 
in the completed gray stage, between the fourth and the 
twenty-fifth day. 

Resolution occurs in spots at first. Fatty degeneration 
and liquefaction of the exudate occur, allowing of its absorp¬ 
tion and expectoration. Resolution should begin soon after 
defervescence, but it may be delayed. 

The unaffected portion of the lung may be congested and 
oedematous, especially the portions near the affected area. 
The bronchi of the pneumonic lobe show catarrhal inflam¬ 
mation, and they may be filled by fibrinous plugs. 

Modifications of the Lesion .—Resolution may be delayed, 
the lung remaining in dry gray hepatization for weeks. The 
exudate may be so excessive that the blood-vessels are 
compressed, leading to necrotic changes of portions of the 
lungs. There may be an excessive production of pus-cells, 
which infiltrate the connective-tissue septa, forming small 
abscesses or a diffused suppuration. Gangrene of the lung 
may occur. Instead of resolution the exudation may be¬ 
come organized into connective tissue, so that the air-cells 
are obliterated and rendered permanently unfit for use. The 
bronchitis may be general and excessive, especially in cases 
accompanying epidemic influenza. 


328 MANUAL OF THE PRACTICE OF MEDICINE. 

Complicating lesions result from infection of other parts 
by diploccoci. Pleurisy is only to be considered a compli¬ 
cation if it extend beyond the pneumonic area or if serous 
or purulent effusion occur. 

Pericarditis is not infrequent. It occurs more commonly 
with double or left-lung pneumonias and in children. It is 
due to diplococcus infection, producing plastic inflammation 
or serous or purulent effusion. The prognosis of pleurisy 
and pericarditis of pneumonic origin is better than that of 
the other forms. 

Endocarditis is more common than pericarditis. It may 
be either simple or malignant; it occurs as an acute exacer¬ 
bation not infrequently in those who have old valvular 
disease. 

Meningitis may occur, and it is usually associated with 
malignant endocarditis. It is often difficult to tell whether 
pneumonia or meningitis be the primary disease. Croupous 
gastritis or colitis may occur. The liver and the kidney 
usually show parenchymatous changes. 

Symptoms .—Prodromal symptoms , consisting of malaise, 
dull pain in the back and the bones, and some soreness in 
the chest, are present in about one-fourth of the cases. 
They last for a day or so, and probably are due to a pro¬ 
tracted stage of congestion. 

The actual onset of the disease is marked by one or more 
chills in about 90 per cent, of the cases, and from the chill 
the duration of the disease is reckoned. In children convul¬ 
sions or vomiting may replace the chill. In old people a 
shivering attack and pain in the side may be the only 
symptoms. 

The temperature rises rapidly and attains its maximum in 
from twenty-four to thirty-six hours, although in some cases 
the height of the fever is not reached until the day before 
defervescence. The fever remains high with slight evening 

o o o 


LOBAR PNEUMONIA. 


Plate 19 



Lobar pneumonia terminating by crisis on the seventh day : temperature (black), pulse 

(blue), and respiration (red). 



Temperature chart of a fatal case of pneumonia: temperature (black), pulse (blue), and 

respiration (red). 























































































































































































































LOBAR PNEUMONIA. 329 

exacerbations, which in uncomplicated cases should not ex¬ 
ceed 104° F. 

Defervescence may occur at any time between the second 



and the eighteenth day, the seventh, fifth, eighth, sixth, and 
ninth days being the favorites, in the order named. The tem- 













Day of 
Disease 

3 

4 

5 

6 

7 

8 

9 

10 



108 c 

105 c 

104° 

103° 




















• 




















1 

DI 

ID*. 



* 


> 




: 














•J 

n 









/ 


wf 




/ 



/ 

s 


7 


V 


s 
















t 



w 



V 



























• 






- 






' 


Fig. 28.—Temperature chart of pneumonia with purulent inflammation terminating fatally. 

perature may fall in from six to forty-eight hours by crisis, 
or in from three to five days by lysis. In some cases the 

















































































































































330 MANUAL OF THE PRACTICE OF MEDICINE . 

temperature is markedly remittent at any time in its course, 
especially in children. In other cases a pseudo-crisis occurs 
about the fifth day. At the time of the crisis the tempera¬ 
ture may fall to subnormal, and after the crisis a slight rise 



Fig. 29.—Lobar pneumonia in child, with remittent temperature (Holt). 


of fever is noticeable for two or three days, especially in 
the evening. A high temperature persisting for ten days 
suggests purulent infiltration or empyema. A sudden rise 



Fig. 30.—Lobar pneumonia; defervescence; gangrene of lung. 


of temperature at any time indicates a complication or an 
extension of the disease. In old people the temperature 
may be normal or even subnormal. In the pneumonias 
complicating epidemic influenza the temperature does not 
























































































































LOBAR PNEUMONIA. 


331 


become normal for days, and it may even persist after reso* 
lution. 

The character of the heart's action is of the utmost import¬ 
ance, as heart failure constitutes the greatest danger of 
pneumonia. The pulse should be full and about 100 in a 
favorable case. A pulse over 120 passes the safety limit and 
gives cause for anxiety. The most critical time is just 
before defervescence, at which time liability to sudden or 
giadual heart failure is the greatest. The possibility of 
sudden death must always be considered. 

In old people rigidity of the arterial walls may give a 
fictitious tension to the pulse, and it is best to note the 
character of the action of the heart itself. Of equal import¬ 
ance with a rapid pulse in old people is an irregular and 
intermittent heart-action. 

A fall in the pulse even to 50 may be noticed before 
crisis. In case of rapid defervescence there may be extreme 
prostration and heart failure. A pulse running up rapidly 
to 140 indicates paresis of the medulla and often precedes 
the fatal issue. In children, however, a rapid pulse is not 
of so much importance, recovery being possible even with 
a pulse of 150 to 200. 

The breathing is rapid and oppressed. Its rapidity varies 
with the amount of fever, the extent of lung involved, the 
severity of pleuritic pain, and the presence of complications. 
The respirations should be below 40 to the minute, a tem¬ 
perature of 104° F., respiration of 40, and a pulse of 120 
being the safety limits. If the respirations be over this 
limit, there should be suspicion of pleuritic effusion or 
pulmonary oedema. 

Dyspnoea may be marked in some cases, especially in 
upper-lobe pneumonias. It is not usually noticed in 
old people, in whom the respiration may not even be in¬ 
creased. 


332 MANUAL OF THE PRACTICE OF MEDICINE. 

Pain in the chest, usually referred to the nipple, occurs in 
85 per cent, of all cases. It is a true pleuritic pain, and it 
does not occur unless the pleura is inflamed. It is a fairly 
constant symptom in old people. 

Cough usually comes early in the disease, but it may be 
deferred until after defervescence, or it may be absent alto¬ 
gether, especially in old people. 

The sputum is scanty, gelatinous, and rusty in color, the 
little pellets sticking to the side of the cup; it is usually 
mixed with the ordinary sputum of bronchitis. This “ rusty 
sputum ” is very characteristic. At the onset there may be 
expectorated a little pure blood. In bad cases there may 
be the “prune-juice” expectoration of an abundant dark- 
brown fluid. This sign is a serious one. In some cases the 
patient will raise casts of the small bronchi that unroll in 
water. In children the sputum is usually swallowed instead 
of being expectorated. 

Cerebral Symptoms. —Headache, restlessness, and sleep¬ 
lessness are frequent; they appear to be due to the pyrexia. 
Delirium belongs to the severe forms of the disease ; it is said 
to be more common in apex pneumonia. In some cases it 
depends upon the pyrexia and is marked by mental wander¬ 
ing, especially at night. In debilitated subjects and in very 
severe cases the symptoms of the “typhoid state ” appear— 
rapid feeble pulse, great prostration, brown dry tongue, and 
a muttering delirium. The last-named symptom is com¬ 
monly seen in alcoholic subjects, who are, moreover, liable 
to develop the typical symptoms of acute delirium tremens. 
Old people are apt to wander in the mind and to evince a 
constant desire to leave their bed and walk about; as a rule, 
however, they are readily controlled. In some non-alcoholic 
adults there maybe acute mania. In children cerebral symp¬ 
toms are more constant, often presenting the clinical picture 
of acute meningitis. Convulsions at the onset may be fol- 


LOBAR PNEUMONIA. 


333 


lowed by headache, photophobia, boring of the head into the 
pillow, convulsive movements, and coma. 

Digestive symptoms are usually not marked. There may 
be nausea and vomiting, especially in alcoholic subjects, and 
in some cases a catarrhal jaundice appears. The bowels are 
usually constipated; the tongue is coated. A brown dry 
tongue belongs to the most severe cases. 

The urine is that of fever, concentrated and depositing 
urates. There is usually a diminished amount of sodium 
chloride, but this sign is not diagnostic. In about one-third 
of the cases albumin and casts are present from a complicat¬ 
ing parenchymatous nephritis, which, however, gives no 
symptoms. It is important to examine the urine in every 
case, to determine the presence of chronic Bright’s disease, 
which adds so grave an element. 

The appearance of the patient is often characteristic. The 
decubitus is usually on the affected side. The expression 
is both apathetic and anxious. There is frequently a well- 
defined mahogany-colored flush on one or on both cheeks 
—not always limited, as was once supposed, to the affected 
side. Herpes labialis occurs in a certain number of cases : 
this sign is to be regarded as a favorable one. The herpetic 
vesicles frequently contain the pneumococci. 

The physical signs may be described as those occurring 
(i) in the stage of congestion, (2) in the stage of consolida¬ 
tion, and (3) in the stage of resolution. 

1. Stage of Congestion .—The normal physical signs are 
the crepitant rale, the subcrepitant rale, a slight dulness, 
and a localized deficiency in chest-expansion. The crepi¬ 
tant rale consists of a shower of fine dry crackles, heard 
directly under the ear at the end of inspiration only. This 
rale was formerly considered pathognomonic of pneumonia, 
and to be due to the inspiratory stretching of the alveolar 
walls stiffened by inflammatory infiltration. It is now con- 


334 MANUAL OF THE PRACTICE OF MEDICINE. 


sidered to be a pure and simple pleural rale, and is con¬ 
sequently present only when the pleura is inflamed. The 
subcrepitant rale may arise either from the rubbing together 
of the inflamed pleurae or from exudate in the small bronchi. 
Slight dulness is apparent by a percussion-note of shorter 
duration, higher pitch, and less resonance than normal. 
Deficiency in chest-expansion is best appreciated by pal¬ 
pation. 



Fig. 31.—Physical signs of lobar pneu¬ 
monia during the stage of congestion: 
slight dulness or dull tympany; breath¬ 
ing feeble or harsh; crepitant and sub¬ 
crepitant pleuritic rales. 


Fig. 32.—Physical signs of lobar pneu¬ 
monia during the stage of complete con¬ 
solidation: dulness; bronchial voice and 
breathing; increased vocal fremitus; crep¬ 
itant and subcrepitant pleuritic rales. 


Exceptional Signs .—There may be a general bronchitis 
with bronchial rales obscuring the physical signs. In these 
cases the disease may be mistaken for bronchitis or for 
tubercular disease. There may be only an area of feeble or 
harsh breathing, with an occasional subcrepitant rale. In¬ 
stead of slight dulness there may be a tympanitic note due 
to relaxation of the congested alveolar walls, or a note of 
mixed tympany and dulness. Should the lesion begin in 
the deeper parts of the lung, physical signs may be absent 
entirely. If the pleura be not involved, the crepitant rale is 
not present. 

2. Stage of Consolidation .—The normal signs are dul- 






LOBAR PNEUMONIA. 


335 

ness, increased vocal fremitus, bronchial voice and breath- 
ing, crepitant and subcrepitant rales, and diminished chest- 
expansion. Dulness is shown by a short, high-pitched 
note of feeble resonant quality, with an appreciable lack 
of resiliency to the percussing finger. Bronchial breath¬ 
ing consists of a harsh, loud, and high-pitched respira¬ 
tory murmur, in which the sound produced by expiration 
is higher pitched and more prolonged than that of in¬ 
spiration. Bronchial voice is high-pitched, loud, and 
nasal in quality. 

Exceptional Signs .—The dulness may have a decided 
tympanitic quality, resembling in some cases even the 

cracked-pot 01 the amphoric note. These modifications 
are more commonly observed in pneumonia of the apex; 
the} nie especially maiked in children. In some cases 
the note may be flat, especially if the bronchi be filled 
with exudate, but the flatness is never so complete as in 
pleural effusion. Should the pneumonic area be small, 
dulness may be obscured by the tympanitic note pro¬ 
duced in the sui rounding lung-tissue by its congestion 
and relaxation. 

Bronchial voice and breathing may be absent. They 
depend upon the flow of air in the bronchi, and they are 
absent if the bronchi are occluded or if the lung does not 
expand with respiration; hence they may be brought out 
by coughing or by deep breathing. 

The crepitant rale may be absent, either because the 
pleura is not involved or because of the poor expansion of 
the lung. Vocal fremitus rarely is diminished or absent. 
If the consolidation begin in the deeper parts of the lung— 
the so-called central pneumonia —the physical signs 
may be delayed for seveial days, making the diagnosis often 
extremely difficult. 

In old people, in whom respiration is feeble, the only 


336 MANUAL OF THE PRACTICE OF MEDICINE. 

physical signs may be the subcrepitant rale and the feeble 
breathing. Dulness is frequently absent in the aged, in 
whom senile changes in the ribs allow of increased res¬ 
onance on percussion. 

3. Stage of Resolution .—The dulness becomes less and less 
marked, bronchial voice and breathing become broncho- 
vesicular and finally normal, vocal fremitus diminishes to 
the normal limit, and moist bronchial rales appear. 

Exceptional Signs .—The dulness may change to tympany, 
which is often the earliest sign of resolution. Crepitant and 

subcrepitant rales, if formerly absent, 
may be heard, from increased lung-ex¬ 
pansion. In some cases the moist bron¬ 
chial rales are not present. Should 
thickening of the pleura persist, slight 
dulness, feeble breathing, and the crepi¬ 
tant rale may be present for a consider¬ 
able time. 

Complications .—Pleurisy with effu¬ 
sion is to be suspected should there be 
disproportional rapidity of breathing, 
and a continuance of fever beyond the 
natural duration of pneumonia. Empy¬ 
ema is marked by the occurrence of 
septic symptoms, erratic chills, irregular 
temperature curve, and sweating. The 
physical signs are those of fluid in the 
pleural cavity, but bronchial voice and 
breathing may be heard below the level of the fluid. In doubt¬ 
ful cases an exploratory aspiration should be resorted to. 

Abscess of the lung occurs in about 1 per cent, of cases, 
from added infection by suppurative microbes. It is usually 
seen in debilitated subjects. Septic symptoms are present. 
There is an expectoration of pus, often fetid, containing 



Fig. 33.—Physical signs of 
lobar pneumonia during the 
stage of resolution : dull tym¬ 
pany or tympany; broncho- 
vesicular voice and breathing, 
becoming harsh, feeble, or 
normal; vocal fremitus, be¬ 
coming normal; crepitant 
and subcrepitant pleuritic 
rales; moist bronchial rales. 





LOBAR PNEUMONIA. 


337 

shreds of lung-tissue, and prostration is extreme. In old 
people there may be no marked symptoms. 

The physical signs are those of pulmonary cavities_ 

tympanitic or “cracked-pot” note, cavernous voice and 
breathing, with moist and gurgling riles. These signs are 
often piesent over a consolidated lung-area containing a 
laige bronchus with adherent pleural surfaces, so that a 
diagnosis by physical signs alone is often impossible. 
Many so-called cases of “abscess of the lung” compli¬ 
cating pneumonia are really acute phthisis with the rapid 
formation of cavities. In doubtful cases a bacterial exam¬ 
ination of the sputum for the tubercle bacillus should be 
made. 

Gangrene of the lung is somewhat less common than 
abscess. Ihe expectoration is a greenish or brownish fluid, 
of fetid gangrenous odor, containing shreds of decomposed 
lung-tissue and crystals of fatty acids. Constitutional symp¬ 
toms are usually pronounced. 

Pericarditis in some cases adds typical symptoms—dysp¬ 
noea, rapid and feeble pulse, venous congestions, and char¬ 
acteristic physical signs. In other cases the diagnosis is 
less evident. Pericardial rales may be simulated by the 
i ubbing together of overlying inflamed pleural surfaces at 
each systole of the heart, and signs of fluid may be obscured 

should the pneumonia involve the overlying portion of the 
lung. 

Endocarditis may be either simple or malignant. The 
latter is to be suspected should septic and embolic symp¬ 
toms be present. Pneumonia occurring in a patient the 
victim ot chronic endocarditis may upset compensation and 
lead to heart failure. During the pneumonia pre-existing 
murmurs of valvular disease may be absent entirely. 

Meningitis may complicate pneumonia with especial 

frequency at different times and in different places. It may 
22 


338 MANUAL OF THE PRACTICE OF MEDICINE . 

run its course with or without typical symptoms. This 
complication may be mistaken for epidemic cerebro-spinal 
meningitis with complicating pneumonia, for tubercular 
meningitis with lesions in the lungs, and for uncomplicated 
pneumonia in children with marked cerebral symptoms. 

Pulmonary oedema usually ushers in the fatal issue. The 
heart failing, the right ventricle becomes more and more 
distended, with consequent congestion and oedema of the 
lungs. The pulse becomes rapid and feeble ; respirations 
are shallow, rapid, and attended by noisy bubbling sounds. 
The expectoration becomes profuse and frothy, and it may 
be blood-stained. Signs of deficient aeration of blood 
appear, and consciousness is lost some few hours before 
death. 

Sudden heart failure may occur at any time, even after 
defervescence. The most usual time is about the time of 
crisis. In some cases thrombosis of the coronary or of the 
pulmonary artery may be found ; in other cases there seems 
to be no assignable cause. 

'Chronic interstitial pneumonia , or fibroid induration, may 
in rare cases result from the organization of the inflamma¬ 
tory exudate into connective tissue, rendering the affected 
area of lung permanently consolidated. 

Prognosis. —The average mortality in hospital cases 
ranges about 25 per cent.; it is somewhat less in private 
practice. Pneumonia of the apex, an extensive lesion, and 
old age render the outlook serious, and the complications 
increase the mortality to a considerable degree. Alcoholism 
must be considered in making the prognosis. According to 
the New York Hospital records, the mortality in non-alco¬ 
holic cases was 25 per cent.; in slightly alcoholic subjects, 
33 per cent.; in those with a marked alcoholic history, 72 
per cent. Patients subject to chronic Bright’s disease are 
apt to die, especially if they be addicted to alcohol. At 


LOBAR PNEUMONIA . 


339 


the New York Hospital 4 such patients recovered and 36 
died. The earlier the patient is put to bed, the better is the 
prognosis. 

Treatment.—Pneumonia is a self-limited disease and 
has no specific medication. In many cases no medicines at 
all are required. The patient should be kept in bed until 
at least five days after the temperature has become normal, 
and on a liquid or light diet. Restlessness and sleepless¬ 
ness 'may be controlled by phenacetine, sulphonal, chloral- 
amide, or by a Dover’s powder given at night. Pain in the 
side may be relieved by hot poultices or by a hypodermic 
injection of morphine. Poultices need not be applied, how¬ 
ever, as a routine measure; in fact, many patients are more 
relieved by cold applications to the chest by ice-bags—a 
treatment which appears to exert a beneficial effect upon 
the disease itself. 

All attempts to abort the disease have proved futile. 
Large doses of calomel—from 25 to 40 grains placed dry 
011 the tongue—seem to exert a beneficial effect upon the 
course of the disease in some cases, producing a sedative 
effect, but there is always the risk of producing salivation. 
Venesection at the outset in robust subjects with pro¬ 
nounced inflammatory symptoms is often of the greatest 
service, relieving the dyspnoea and the cerebral symptoms 
and reducing the fever. In the later stages, when the heart 
is beginning to fail, and cyanosis and symptoms of dilata¬ 
tion of the right ventricle appear, venesection may be em¬ 
ployed as a last resort. 

As an arterial sedative tincture of aconite of tincture of 
veratrum viride has seemed to be of service if given at the 
outset, but in robust patients venesection is preferable. 

The temperature, being of relatively short duration, rarely 
requires much treatment. The use of internal antipyretics 
as a routine is to be deplored, on account of their depressant 


340 MANUAL OF THE PRACTICE OF MEDICINE. 


effect. High and prolonged temperature should, however, 
be controlled. For this purpose hydrotherapy is the best 
treatment to be employed—either cold sponging, the cold 
pack, cold applications to the chest, or even the bath at 70° 
F. By the use of the bath the temperature is reduced, the 
pulse becomes stronger, and cerebral symptoms are markedly 
relieved. 

By far the most important treatment is that to sustain the 
action of the heart. Should the pulse become rapid and 
feeble and the second pulmonary sound weak, alcohol 
should be given freely, in doses sufficient to accomplish 
the end desired. In the aged and in alcoholic subjects it 
should be given from the start. The use of digitalis is 
frequently disappointing from its contractile power over 
the small arteries, unless it be combined with an arterial 
relaxant, such as nitroglycerin or iodide of potassium. A 
good combination is— 

I^. Potassii iodidi, gr. v ; 

Ext. digitalis fluid., Tffj; 

Ext. convallariae fluid., Tffxx.—M. 

Sig. Such a dose every three hours. 


As a cardiac tonic strychnine is rapidly gaining in favor. 
It may be combined with digitalis and aconitine with advan¬ 
tage, as in the following prescription : 


R. Strychnine sulphate, 
Digitaline, 
Aconitine, 


g r * 6T 1 
S r - rhr 5 

err _I_ 


Such a combination in pill form may be given every two or 
three hours until the pulse is reduced to about 100, but 
with such a form of treatment the patient should be watched 
carefully. Ammonia or camphor may also be employed. 



BRONCHO- PNE UNION I A. 


341 


Should heart failure with increasing difficulty of breathing 
occur, free stimulation, cupping of the chest, and the admin¬ 
istration of pure oxygen gas should be employed ; in some 
cases tree venesection proves satisfactory. 

Complicating delirium tremens calls for free stimulation, 
for sedatives such as bromide, chloral, or hypodermic injec¬ 
tions of morphine, and frequently for physical restraint. 
The sedative and tonic effect of the cold bath is often sur¬ 
prising in these cases. 

Expectorants serve only to upset the stomach, although 
in some cases of tardy resolution pilocarpine may be em¬ 
ployed, its depressant effect being carefully guarded by 
stimulants. 

Experiments recently made by Drs. G. and F. Klemperer 
upon the toxines of pneumonia are of wonderful and vital 
interest. These observers found that rabbits could be 
rendered immune by hypodermic injections of heated pneu¬ 
mococcus cultures, and that the blood-serum from these 
labbits, injected into patients suffering from pneumonia, 
Produced an immediate curative effect upon the disease. 
More recently the blood-serum of patients who had just 
passed the time of crisis has been used for the injections, 
with equally brilliant results, the theory being that the serum 
from immune animals or from convalescent patients contains 
an antitoxine capable of neutralizing the toxine caused bv 
the growth of the pneumococcus in the body. The latter, 
known as “ pneumotoxine,” has already been isolated, but 
the supposed antidotal toxine, the “ antipneumotoxine,” has 
not as yet been obtained in a chemically pure state. 

BRONCHO-PNEUMONIA. 

Eitolog*y and Synonyms.—Broncho-pneumonia is the 
legular pneumonia of young children, but it may be seen 
in adults, and it is not uncommon in old people. Primary 


342 MANUAL OF THE PRACTICE OF MEDICINE. 

cases follow exposure to wet and cold or the inhalation of 
irritating chemical vapors; they are more common in the 
winter and spring months and among the debilitated tene¬ 
ment-house and asylum children. Secondary cases accom¬ 
pany many of the infectious diseases, especially measles, 
scarlet fever, whooping-cough, and diphtheria. Broncho¬ 
pneumonia may occur in any disease which keeps the 
patient in bed, the dorsal decubitus preventing free expec¬ 
toration, and the foul mouth of fevers allowing the growth 
of bacteria in the mouth. The bacteria enter the lung 
with the inspired air and infect it. Careful cleansing of the 
mouth in prolonged fevers will often prevent the occurrence 
of this so-called “ aspiration- ” or “ inhalation-pneumonia.” 
“ Deglutition-pneumonia ” is that form of pneumonia pro¬ 
duced by the passage of food or drink into the bronchi 
from choking at table, in deep coma, or from tracheotomy, 
intubation, or cancer of the larynx or the oesophagus. 
Suppuration or even gangrene may result in such cases. 
Patients with advanced emphysema are liable to subacute 
attacks of broncho-pneumonia. Tubercular broncho-pneu¬ 
monia will be considered under a separate heading. Bron¬ 
cho-pneumonia may be produced either by the ordinary 
pneumococcus or by the streptococcus of suppuration. 
Synonyms: Lobular pneumonia; Catarrhal pneumonia; 
Capillary bronchitis. 

Pathology. —The lesion consists of a bronchitis and a 
pneumonia. The bronchitis is general, involving the bronchi 
of both lungs. The large, the medium, and the smallest 
bronchi are all involved, although not always to the same 
extent. The mucous membrane of the bronchi show ordi¬ 
nary catarrhal inflammation; the walls of the smallest 
bronchi are thickened by an infiltration of new cells, and 
may be dilated ; the smaller bronchi may contain pus. The 
pneumonia differs from lobar pneumonia in the location 


BR ONCHO- PNE UMONIA . 


343 


of the affected areas and in the regular involvement of the 
connective-tissue walls of the air-cells. Around the bronchi 
are zones of consolidated lung-tissue, varying in size from 
a pin s head to that of a pea. These areas of peri-bron- 
chitic hepatization may be so slight as almost to escape 
notice, so that the lesion appears to be bronchitis alone. 
These cases were formerly described as “capillary bron¬ 
chitis.” In other cases the areas are larger, so that the 
lungs are filled by these isolated nodular bodies; while in 
yet other cases, the “ pseudo-lobar form,” the areas are large 
and confluent, so that the greater part of the lobe is 
rendered solid. The cut surface of a broncho-pneumonic 
patch is smooth, lacking the granular appearance of the 
hepatization of lobar pneumonia. Gray hepatization is but 
rarely seen. 

Microscopic examination shows the air-spaces filled with 
fibrin, pus, epithelial cells, and red blood-cells. 

In children there is a relatively greater proportion of 
epithelial cells in the exudate than in adults. The walls 
of the air-spaces are thickened and are infiltrated by small 
round cells or by fibrin, pus, and epithelium. 

The lung-tissue between the nodules may be either nor¬ 
mal or congested and cedematous, or it may be the seat of 
a diffuse pneumonia in which the air-spaces are partially 
filled with fibrin, pus, epithelial cells, and red blood-cells, or 
the air-spaces may be collapsed. These areas of collapse or 
atelectasis are depressed below the surrounding tissues and 
are of a bluish or blue-brown color. These areas may be 
small and may only surround the peribronchitic nodules, or 
the greater part of a lobe may be involved. In recent 
cases the air-spaces may be inflated by a blow-pipe inserted 
into the bronchus leading to them. 

The pleura covering the peripheral pneumonic patches is 
covered with fibrin. The bronchial glands are almost 


344 MANUAL OF THE PRACTICE OF MEDICINE. 


always swollen and inflamed. This condition may persist, 
rendering the glands susceptible to an added tubercular 
infection, from which systemic infection may result. Many 
cases of tuberculosis in asylums follow epidemics of 
measles, the sequence being measles, broncho-pneumonia, 
inflammation, tubercular infection of the inflamed bronchial 
glands, general miliary tuberculosis. 

There is a common misapprehension that the inflamma¬ 
tion extends from the bronchi into the air-spaces which 
open into them. In point of fact, it is the air-spaces sur¬ 
rounding the axis of the bronchi that are involved. If hot 
knitting-needles be run into a loaf of bread, the path of 
each needle will represent a bronchus, while the charred 
bread surrounding its track will represent the position of 
the peribronchitic pneumonia. 

The interstitial inflammation of the walls of the bronchi 
and the air-spaces is a special feature of broncho-pneumonia. 
It is of especial importance from its tendency to become 
chronic, by the changing of the infiltrating cells into devel¬ 
oped connective tissue. 

Symptoms .—In young babies fever, prostration, and rapid 
breathing are the only constant symptoms. There may be 
no cough, and physical signs are not present. The disease 
runs almost regularly a fatal course within a few days. 

Mild cases in children may resemble severe ordinary 
bronchitis. In broncho-pneumonia the general symptoms, 
however, are more severe, and the physical signs point 
to an involvement of smaller bronchi than in bronchitis 
alone. A temperature of 102.5 0 or 103° F. persisting 
for three days gives evidence of more than a simple bron¬ 
chitis. 

Severer forms in children may begin gradually or abruptly 
—gradually by the extension of a simple bronchitis, or 
abruptly by convulsions or vomiting. Should the pneu- 


Bronchopneumonia : prolonged course ; recovery. 



BRONCHO-PNEUMONIA. Plate 20 . 














































































































BR ONCHO-PNE UMONIA. 345 

monia be secondary to some well-marked infectious disease, 
the onset is somewhat obscured. 

When the disease is established there is a fever which is 
usually remittent in character, often markedly so. There is 
no typical curve, as in lobar pneumonia, and there is no day 
of crisis. The height of the fever is often proportional to 
the severity of the attack, but some patients do badly whose 
temperature ranges between 99 0 and ioo° F. The circum¬ 
stances under which these low temperatures are met with are 
early infancy, low vitality, and great prostration with little 
reactionary power. The pulse becomes rapid, frequently 



Fig. 34.—Typical broncho-pneumonia of the milder form (Holt). 


ranging from 140 to 180 in many children. Respirations 
may be as high as 50 to 80 to the minute, and they are 
marked by inspiratory dilatation of the alae nasi. There is 
often an expiratory moan or grunt. There may be audible 
bronchial rales. The dyspnoea may make it difficult for 
the child to nurse. There is frequently cough, which may 
be painful. The sputum is that of bronchitis; it is usually 
swallowed, but it may be vomited up. Rusty sputum is 
not present. In older children the sputa may be blood- 
streaked. The face is flushed, the skin is dry, the tongue is 
coated; vomiting is frequent, and it may interfere with the 
proper feeding of the child. There may be restlessness, 
sleeplessness, or mild delirium, depending on the fever and 
the disposition of the child. The urine may contain small 
amounts of albumin and casts. In cases developing during 




























346 MANUAL OF THE PRACTICE OF MEDICINE . 

some severe disease, constitutional symptoms may be 
obscured, the rapid breathing alone attracting attention 
to the lung. 

Cerebral Cases .—There are cases in which the cerebral 
symptoms may be so pronounced as to obscure those of 
pulmonary origin. There may be headache, repeated con¬ 
vulsions, delirium, photophobia, retraction of the head, and 
muscular twitchings. Pulmonary symptoms appear later in 
the disease in the majority of cases, with a subsidence of 
the cerebral symptoms. The diagnosis from meningitis in 
many cases is difficult. The points in favor of pneumonia 
are absence of tuberculosis or of suppurative ear disease, a 
higher respiration-rate, absence of paralysis, a more rapid 
pulse, and the presence of physical signs. The cerebral 
symptoms, moreover, are neither so severe nor so con¬ 
tinuous as in meningitis, and they disappear with defer¬ 
vescence. 

Physical Signs.—In all cases signs of bronchitis are 
present—coarse and subcrepitant rales, especially at the 
bases, with sibilant and sonorous breathing. If the pneu¬ 
monic patches be small and scattered, there may be no 
added signs, so that the diagnosis from bronchitis will be 
made by other means. If the pneumonic patches be larger 
and nearer one another, there will be a tympanitic or dull note 
with harsh breathing. If the patches so coalesce as to 
involve a larger area, there will be dulness, bronchial voice 
and breathing, and increased vocal fremitus. Fibrin on the 
pleura gives rise to crepitant and subcrepitant rales of super¬ 
ficial quality. 

Course and Termination.—The disease may terminate— 
(i) In resolution. The disease continues for from two to 
three weeks in the majority of cases, the temperature fall¬ 
ing by lysis. In some cases the symptoms continue for 
from six to eight weeks before recovery. Resolution is 


BR ONCHO- PNE UMONIA. 


347 


slower than in lobar pneumonia, being rarely completed in 
less than from seven to fourteen days. 

(2) In death from asphyxia. In cases that are doing 
poorly the dyspnoea becomes more distressing, the skin is 
bluish, and the pulse becomes more and more rapid and 
feeble. As the child gradually succumbs to carbon-dioxide 
poisoning the dyspnoea becomes less apparent, distress gives 
way to stupor alternating with restlessness, the cyanosis 



Fig. 36.—Broncho-pneumonia: zones of 
peribronchial consolidation more extensive ; 
physical signs of general bronchitis and 
of small localized areas of consolidation. 


Fig. 35.—Broncho-pneumonia : zones 
of peribronchial consolidation very slight ; 
physical signs of bronchitis (“capillary 
bronchitis ”). 


deepens, the bronchi fill with mucus, and death results from 
heart paralysis. 

(3) In suppuration or gangrene. Either termination is 
rare except in the aspiration and deglutition forms. 

(4) In chronic interstitial pneumonia. In these cases the 
cells infiltrating the walls of the bronchi and of the air-cells 
become organized into connective tissue. In this way the 
walls of the bronchi are thickened and dilated and are sur¬ 
rounded by zones of connective tissue that represent the 






348 MANUAL OF THE PRACTICE OF MEDICINE. 


former areas of peribronchitic pneumonia. By the coales¬ 
cence of these zones more or less of the lung is rendered 
permanently unfit for use. The pulmonary pleura is usually 
much thickened. Such a lung is exceedingly apt to develop 

tubercular changes in the course of 
time. 

In some cases the pneumonia 
runs an acute course, and in one or 
two weeks the temperature falls and 
the child becomes better but cannot 
be said to be actually convalescent. 
There continues to be a moderate 
irregular fever; the cough contin¬ 
ues and emaciation becomes more 
marked. 

After a few months some of these 
cases recover, though with small 
*ig. 37 ; —Broncho-pneumoma : areas of interstitial pneumonia which 

peribronchial consolidation exten- 1 

sive, giving the physical signs of may give no further trouble or 

which may cause repeated attacks 
of bronchitis, while in other chil¬ 
dren tuberculosis develops, either from infection from tuber¬ 
cular bronchial glands or from a local infection of the dis¬ 
abled lungs by the tubercle bacillus. 

In other cases the fever, cough, and emaciation continue, 
hectic develops, and the child dies emaciated and exhausted. 
The course of the disease is that of chronic pulmonary 
phthisis, but at the autopsy there is found extensive inter¬ 
stitial pneumonia with large bronchiectatic cavities. 



consolidation of large areas, re¬ 
sembling lobar pneumonia. 


Broncho-Pneumonia in Adults. 

The disease in adults presents a variety of clinical forms 
which are thus described by Delafield : 

I. There is first ordinary bronchitis for several days, but, 





BR ONCHO- PNE UMONIA. 


349 

instead of recovering, the patient continues to cough and to 
feel sick, and at some part of the chest there is found a 
small area of dulness and high-pitched voice. The consoli¬ 
dation lasts but a short time, and the patient regularly 
recovers. 

2. The patient is seized by a chill; there are rapid and 
high fevei, pains in the back and the chest, great prostra¬ 
tion, rapid and feeble pulse, rapid and insufficient breathing, 
cough with mucous and blood-stained sputa, sleeplessness, 
lestlessness, and delirium. The urine contains albumin and 
casts; the skin is cyanosed; the viscera are congested. 
Ov ei both chests the percussion-note is normal, exagger¬ 
ated, or dull. Coarse subcrepitant and crepitant rales with 
sibilant and sonorous breathing are heard. The disease 
lasts for one or two weeks and is apt to prove fatal. 

3. A lorm of broncho-pneumonia resembles lobar pneu¬ 
monia. Fheie is a general bronchitis, with broncho-pneu¬ 
monia and consolidation of one or more lobes. Compared 
with lobar pneumonia, the invasion is more gradual, the 
pulse is more rapid, cerebral symptoms are more constant, 
the sputum is that of bronchitis, the physical signs are 
delayed in their appearance, the duration is longer, and 
resolution is slower. 

4. A form resembles tubercular broncho-pneumonia. 
The invasion is gradual and the disease is protracted for 
weeks. T. he patients have fever with evening exacerbations 
and night-sweats, cough with muco-purulent expectoration 
which does not contain tubercle bacilli, and there is a loss 
of flesh and of strength. Physical signs show bronchitis 
with localized areas of consolidation. Some patients re¬ 
cover after a number of weeks j in others the disease proves 
fatal. 

5. Patients with emphysema may develop a subacute 
broncho-pneumonia which is often fatal. 


350 MANUAL OF THE PRACTICE OF MEDICINE. 


6. Broncho-pneumonia, especially of the lower lobes, may 
be seen in infectious diseases, injuries, and operations which 
cause congestion of the lungs and allow of the inhalation of 
streptococci. 

The prognosis depends—(i) Upon the age. The disease 
is generally fatal in young infants. The mortality is 50 per 
cent, under one year, 40 per cent, between the first and the 
third year, and 25 per cent, between the third and the fifth 
year. (2) Upon the severity of the attack. Mild cases may 
be no more fatal than bronchitis. (3) Upon the general nutri¬ 
tion of the child, being worse in asylum- and tenement- 
house cases. (4) Upon the nature of the primary disease, 
being worse with whooping-cough, measles, or diphtheria. 
Aspiration- and deglutition-pneumoniasare usually severe. 
An absolute prognosis should never be made, as the sickest 
child may recover and apparently mild cases may do badly. 

The prognosis in cases of chronic broncho-pneumonia 
depends upon the amount of lung disabled, the possibility 
of avoiding tubercular infection, and the care that can be 
taken of the case. 

Treatment. —Much can be done to prevent the disease. 
Convalescent fever patients, and especially those convales¬ 
cing after measles or whooping-cough, should be guarded 
carefully from catching cold. All bronchial affections in 
young children and in the debilitated and the aged should 
be attended to properly, especially in the winter and spring 
months. The mouth and the teeth of all fever and bed¬ 
ridden patients should be kept scrupulously clean by fre¬ 
quent washings with antiseptic solutions. Hypostatic con¬ 
gestion is to be prevented by occasional change of position 
in bed. 

In general terms, the treatment of broncho-pneumonia 
is that of lobar pneumonia, except that the patient is 
usually a young child and that the bronchitis is an additional 


BR ONCHO-PNE UMONIA . 


351 


feature. There is, moreover, less danger of heart failure 
than in lobar pneumonia. The patient should be put to 
bed in a room having a temperature of about 68° or 72 0 F., 
the air being kept moist by a steam-kettle or an atomizer. 
The diet should be fluid during the febrile stage, and the 
patient should be allowed cool water sufficient to quench 
the thirst. At the outset the bowels should be opened, 
calomel (gr. ^ every hour until an movement occurs) being 
generally advisable. For the febrile symptoms an ordinary 
saline fever-mixture may be employed, such as citrate of 
potash, liquor ammoniae acetatis, or spiritus setheris nitrosi. 
If there be high fever with bounding pulse, minim doses of 
tincture of aconite may be employed every 1 to 3 hours. 
Internal antipyretics are not to be recommended. Should 
the fever need reduction, it is best to employ the cold bath 
or the wet pack, beginning with a tepid temperature and 
gradually reducing it to 8o° or 75 0 F. 

For the bronchitis counter-irritation may be applied to the 
chest by turpentine and sweet oil, by mustard poultices 
made thin and light, or by chloroform liniment. The chest 
may be covered with the oil-silk jacket, which consists of a 
flannel shirt over which are sewn strips of oil silk. Poul¬ 
tices are heavy and are not so much employed now as 
formerly. Expectorants are to be given in the majority of 
cases, as in simple bronchitis, but disturbance of the stomach 
and continual nausea should be avoided. If the child has 
trouble in bringing up the mucus, an occasional emetic is 
often valuable, provided the heart be acting well. 

In commencing asphyxia and heart failure inhalations of 
pure oxygen gas are to be recommended, and vigorous 
heart-stimulation is to be employed, digitalis, strychnine, 
and small doses of brandy being used for this purpose. Un¬ 
der these circumstances a hot mustard bath for the entire 
body is often beneficial. 


352 MANUAL OF THE PRACTICE OF MEDICINE. 

Pain and distressing cough frequently require small doses 
of Dover’s powder or codeine, but opium must be given 
with extreme caution to young children. 

Cerebral symptoms are best treated by phenacetine, so¬ 
dium bromide, or chloral, and by the cold pack. If resolu¬ 
tion be delayed or if the danger of a persistent interstitial 
pneumonia threaten, a vigorous tonic treatment of iron, 
quinine, and cod-liver oil is to be employed, with strict 
attention to the diet and the assimilation of food. Should 
these means prove inoperative, a change of air is advisable. 


INTERSTITIAL PNEUMONIA. 

Definition. —Interstitial pneumonia is a chronic inflam¬ 
mation of the connective-tissue framework of the lung, 
resulting in the production of new connective tissue and the 
obliteration of the air-spaces. 

Etiology. —The disease is part of the lesion of chronic 
pulmonary phthisis, of syphilitic pneumonia, and of sub¬ 
stantive emphysema. It occurs as the result of chronic 
bronchitis, pleuritic adhesions, broncho-pneumonia, lobar 
pneumonia, and the continual inhalation of solid particles 
in the air in various occupations. To the disease caused by 
inhalation the term “ pneumonokoniosis ” has been applied, 
while special names are given according to the nature of the 
inhaled particles: Anthracosis , due to the inhalation of coal- 
dust; siderosis, due to iron-dust; clialicosis, due to stone- 
dust, etc. The names of various occupations have also 
been attached, such as “ miners’ phthisis,” “ millers’ lung,” 
“masons’ lung,” “stone-cutters’ phthisis,” “grinders’ rot,” 
etc. 

Pathology. —The lesion consists in the growth of connec¬ 
tive tissue which replaces the normal lung structure. The 
walls of the air-spaces and of the bronchi are usually first in¬ 
volved by connective-tissue thickening, so that the air-spaces 


INTERSTITIAL PNEUMONIA. 


353 


are diminished in size, are frequently deformed by polypoid 
projections into them of connective tissue, and may be 
effaced entirely. The walls of the bronchi, losing their 
elasticity, may dilate to form bronchiectatic cavities whose 
lining may be mucous membrane, connective tissue, or a 
suppurating surface. Similar connective-tissue changes are 
usually seen in the pleura, which becomes thickened and 
adherent. 

The new connective tissue, having scanty blood-vessels, 
replaces vascular lung-tissue, so that, the number of blood- 
channels between the right and the left heart becoming 
reduced, there may either be a compensatory hypertrophy 
of the right ventricle, or its dilatation with general venous 
congestions. The unaffected portions of the lung are apt 
to be emphysematous. 

The appearance of the lung varies with the cause of the 
pneumonia. 

1. Interstitial Pneumonia due to the Inhalation of Dust .— 
The connective tissue thickening occurs in the walls of the 
bronchi and of the surrounding air-spaces. Later there 
may be areas of different interstitial pneumonia, rendering 
more or less of the lung solid. The affected areas are 
stained by the deposit of the irritating dust-particles; the 
bronchial glands are inflamed and contain the offending par¬ 
ticles. Bronchiectatic cavities frequently occur. 

2. Interstitial Pneumonia following Broncho-pneumonia .— 
Here the chronic lesion follows the localities of the acute 
form. The walls of the bronchi are involved and frequently 
are dilated; there are peribronchial fibrous nodules, with 
occasionally diffused areas of interstitial pneumonia. The 
process may be entirely peribronchial or it may involve a 
whole lobe. 

3. Interstitial Pneumonia due to Lobar Pneumonia .—These 
are the rare cases in which the exuded products in the air- 

23 


354 MANUAL OF THE PRACTICE OF MEDICINE. 

spaces become organized, so that the lobe is rendered 
permanently solid. 

4. Interstitial Pneumonia following Chronic Pleurisy .— 
In this form the pleura is much thickened, and from it bands 
of connective tissue pass into the substance of the lung. 

5. Interstitial Pneumonia following Chronic Bronchitis .— 
Here the walls of the bronchi are thickened and dilated 
with fibrous nodules about the bronchi. 

The symptoms begin gradually. There is a chronic 
bronchitis with a cough and with mucous or muco-purulent 
expectoration which may be fetid. There may be small 
repeated haemoptyses. If there be bronchiectatic cavities, 
the expectoration will be more profuse, and from time to time, 
frequently after bending over or after any change in posi¬ 
tion, a large quantity of secretion will be expectorated. 

Fever is not present except during acute exacerbations of 
the bronchitis and from suppurating bronchiectatic cavities. 
In the latter case the fever may assume the hectic type, 
with night-sweats and emaciation similar to the septic symp¬ 
toms so commonly observed in pulmonary phthisis. 

Pain in the chest is common if the pleura be involved. 
Dyspnoea is usually present, depending upon the extent 
of lung involved and the condition of the right heart. 
Should dilatation of the right heart occur, there will be the 
general venous congestions regularly observed in this con¬ 
dition. 

The physical signs vary according to the actual condi¬ 
tion of the lung. The bronchitis gives rise to coarse and 
subcrepitant rales with sibilant or sonorous breathing. 

The fibrous areas give the regular signs of consolidation— 
dulness on percussion, increased vocal fremitus, and bron¬ 
chial voice and breathing. If the areas be small, the note 
may be tympanitic and the breathing sounds may be feeble 
or harsh or broncho-vesicular. 


interlobular emphysema. 


355 


Dilatation of the bronchi gives rise to the physical signs 
of cavities tympanitic or “ cracked-pot ” note, more rarely 
a note of amphoric quality, with cavernous breathing, inten¬ 
sified voice, and bubbling rales of large size. 

The thickened pleura causes dulness or flatness on per¬ 
cussion, while vocal fremitus, breathing, and voice are 
diminished or lost. There are also creaking, rubbing fric¬ 
tion-sounds of all kinds. 

From shrinkage of the connective tissue the affected areas 
are reduced in size, so that there is a retraction of the chest- 
wall and limited respiratory expansion, in strong contrast to 
the unaffected side. There may be overlapping of the ribs 
and spinal curvatures. The heart may be displaced by 
being drawn to the affected side, or the area of impulse may 
be abnormally visible should the lung over it be retracted. 

Prognosis. The disease lasts for years, the more severe 
cases being semi-invalids. There is always danger of an 
added tubeicular infection, to which these lungs are exceed- 
ingly liable. If large areas of lung are involved, there is 
always danger of dilatation and failure of the power of the 
right heart. Patients, moreover, are apt to do badly if they 

develop acute inflammation of the remaining portions of the 
lung. 

Treatment.—The only thing that can be done is to send 
the patient to a mild climate where the bronchitis will not 
b e aggiavated by exposure to cold and dampness. If this 
cannot be done, the general nutrition of the patient should 

be improved in every way, and the chronic bronchitis 
treated. 


INTERLOBULAR EMPHYSEMA. 

Etiology.—Interlobular emphysema usually follows severe 
expiratory efforts, as in whooping-cough, and is most fre¬ 
quently seen in the broncho-pneumonia of young children. 


356 MANUAL OF THE PRACTICE OF MEDICINE. 

The disease has also occurred as the result of straining 
efforts with closure of the glottis in parturition, excessive 
muscular exertions, and convulsions. 

Pathology.—By rupture of the air-spaces air escapes 
into the interlobular septa, rupturing into the pleural cavity 
to cause pneumothorax, or extensively infiltrating the con¬ 
nective-tissue septa and compressing the parenchyma of the 
lung. In rarer cases it may make its way into the medias¬ 
tinum and extend up the course of the trachea to the sub¬ 
cutaneous tissues of the neck. 

The symptoms are not distinctive. Pneumothorax may 
result, and severe cases may be followed by sudden death. 

VESICULAR EMPHYSEMA. 

There are three distinct forms of vesicular emphysema— 
compensatory, substantive, and senile. 

Compensatory Emphysema. —When part of the lung is 
so disabled that it cannot expand fully, the remaining por¬ 
tions have to expand or the chest-wall will fall in. Com¬ 
pensatory emphysema consists, then, simply in an over¬ 
stretched condition of the lung, with distended air-vesicles 
whose walls are thinned. It occurs as a temporary con¬ 
dition in pneumonia, broncho-pneumonia, and with pleuritic 
effusions. When the cause is more permanent, as with 
phthisis, pleural adhesions, and interstitial pneumonia, 
groups of air-vesicles may remain permanently distended. 
This form is a normal compensatory process, gives no 
symptoms, subsides with the subsidence of the original 
disease, and is of no practical detriment to the patient. 

Substantive Emphysema. —Etiology.—Much uncertainty 
exists as to the true nature of substantive emphysema. 
Formerly it was regarded as a mechanical over-inflation of 
the lung from forced inspiratory or expiratory efforts. This 
condition argued some weakness of the lung-tissue, so that 


VESICULAR EMPHYSEMA. 


357 


it was supposed that, to account for the over-inflation, there 
must be a congenitally weak lung-tissue; this theory ap¬ 
peared to be borne out by the markedly hereditary char¬ 
acter of the disease. It was found, however, that there were 
cases of emphysema without any dilatation of the air-spaces, 
so that this could not be regarded as an essential feature. 
Delafield describes the disease as a chronic interstitial in¬ 
flammation of the lung, with which condition more or less 
dilatation of the air-spaces is usually, but not invariably, 
associated. His studies have been so extensive and thor- 
ough that his descriptions of the disease process will be 
followed to the exclusion of other theories. 

Pathology. —The lungs are large, downy or feathery to 
the feel, and do not collapse when the chest is opened. 
Enlarged air-vesicles are usually visible, especially along 
the anterior margins, and on the inner surface of the lobe 
near the root of the lung. In some cases, however, there 
is no dilatation of the air-spaces, and these cases may even 
be attended by most marked symptoms of emphysema dur¬ 
ing life. The walls of the air-spaces are thickened in some 
parts of the lungs, thinned in others, and the epithelial 
cells lining them are often increased in size and number. 
Atrophic changes in the walls of the vesicles allow of per¬ 
foration, so that a number of vesicles may merge into a com¬ 
mon air-chamber. With the atrophy of areas of the vesic- 
ulai wall there is a disappearance of the capillaries coursing 
over it, so that the number of channels between the right 
and the left heart becomes materially reduced. In many 
cases there exists a contraction of the smaller arteries, 
which still further increases the pulmonary obstruction. 
The septa between the lobules, the connective tissue around 
the bronchi and the blood-vessels, and the pulmonary pleura 
aie often considerably thickened, and frequently there are 
adhesions between the pleural surfaces. There is regularly 


358 MANUAL OF THE PRACTICE OF MEDICINE. 

a chronic catarrhal bronchitis, but bronchiectasis is not 
common. There may be endarteritis of the branches of the 
pulmonary or bronchial arteries, and it is supposed that 
in many cases spasmodic contraction of these arteries occurs 
during the life of the patient. 

Secondary lesions result from the mechanical obstruction 
to the pulmonary circulation, both from the disappearance 
of some of the capillaries, and also from the contraction of 
the small arteries ; these lesions consist in the hypertrophy 
and dilatation of the right side of the heart. If dilatation 
and heart failure occur, there will be venous congestions of 
the skin, the serous membranes, and the viscera. The con¬ 
dition of the right heart—whether compensatory hypertro¬ 
phy occurs and remains established—is of the greatest im¬ 
portance to the patient. 

Associated lesions are usually found. They consist of 
chronic endocarditis, chronic endarteritis, and chronic 
diffuse nephritis. These lesions depend, as does emphy¬ 
sema, upon the slow production of connective tissue 
replacing pre-existing tissues, and they are therefore apt to 
be associated in the same patient. 

Symptoms. —Of the regular symptoms, dyspnoea is the 
most prominent. At first the dyspnoea is induced only by 
exertion, by indigestion, or by attacks of bronchitis; later 
it becomes more steady and troublesome. Many of the 
attacks of dyspnoea appear to be due to contraction of the 
small arteries of the lung. 

Symptoms of bronchitis are present, especially in the 
winter months. The patient has a paroxysmal, ineffectual 
cough, with muco-purulent expectoration. Exacerbations 
of the bronchitis are accompanied by an increase of the 
cough and the expectoration, and possibly by slight fever, 
night-sweats, and rarely by small haemoptyses. Should 
bronchiectatic cavities form, they are marked by a charac- 


VESICULAR EMPHYSEMA. 


^ * c\ 


teristically profuse expectoration after change of position 
and by physical signs. 

Symptoms of asthma are commonly present; they are 
usually most severe during the exacerbations of the bron¬ 
chitis. 

The respirations are labored and wheezy; expiration is 
unduly prolonged. The obstruction in the pulmonary sys¬ 
tem allows of cyanosis, often of an extreme grade, but it is 
not incompatible with comparative comfort. 

When compensation fails and the right heart dilates, 
general venous congestions are gradually developed—con¬ 
gestion and oedema of the skin, congestion of the stomach, 
the liver, and the kidneys, and general dropsy. 

The symptoms of chronic endarteritis, of chronic endo¬ 
carditis, or of chronic diffuse nephritis may complicate the 
course of the disease and may even obscure the diagnosis. 

Variations in the Course of the Disease. —The follow¬ 
ing clinical types of the disease are described by Delafield : 

“ I. Some patients for years have a winter cough, with ex¬ 
pectoration of mucus and sometimes of a little blood. The)' 
are always a little short of breath when they exert them¬ 
selves. After a time they have attacks of spasmodic asthma. 
Then the dyspnoea on exertion becomes more constant and 
more decided; the patients lose flesh and strength ; venous 
congestion is established, dropsy, and death. 

“ 2. Other patients are fairly well except when they have 
attacks of acute bronchitis. Such attacks may be mild, 
lasting a few days or a few weeks, with cough, mucous ex¬ 
pectoration, sometimes haemoptyses, asthmatic breathing, 
and a febrile movement; or the attacks may be severe, and 
last two or three months, and, in addition to the symptoms 
just mentioned, they develop venous congestion, albumi¬ 
nuria, and dropsy. 

“3. In some patients there is a history of attacks of 


360 MANUAL OF THE PRACTICE OF MEDICINE. 

spasmodic asthma for a number of years before the symp¬ 
toms of emphysema make their appearance. 

“4. In some patients the evidences of emphysema are 
very slight for a long time. Then rather suddenly constant 
dyspnoea and venous congestion are developed, and the 
patients die in a few months.” 

Physical Signs. —Inspection may reveal nothing abnor¬ 
mal. In advanced cases there is an increase in the antero¬ 
posterior dimensions of the thorax, approaching the “ barrel¬ 
shaped chest” in some cases. The chest rises and falls 
en masse and with evident muscular action, dyspnoea being 
evident. Lateral expansion is not well marked. The head 
inclines forward, the shoulders are rounded, the sterno- 
cleido-mastoid muscles are prominent, and the respiratory 
action of the diaphragm is increased. The thorax in em¬ 
physema has aptly been described as one of “ permanent 
inspiration.” 

Pulmonary resonance may be unchanged or vesiculo¬ 
tympanitic, or there may exist an exaggerated resonance of 
a tympanitic quality, or the resonance may be of a variety 
of tympany of a dull quality. This latter note, often called 
“ wooden,” is highly characteristic. The percussion bound¬ 
aries of the lung are increased in all dimensions, and, owing 
to the increased thickness of the covering lung, the borders 
of the heart are determined with great difficulty. 

The characteristic breathing is feeble compared with the 
evident expansion of the chest; the expiration is much 
longer than inspiration, and is of a lower pitch. More 
rarely both inspiration and expiration may be harsh, loud, 
and high-pitched. 

Sibilant and sonorous rales are usually present, and the 
bronchitis adds coarse mucous rales. 

Prognosis. —Substantive emphysema is essentially chronic, 
its course extending over years. Moderate degrees of em- 


t'ESICULAR EMPH YSEAIA. 


361 

physema are not incompatible with prolonged and active 
life, but in each case the questions must be, How much 
extra work is thrown upon the right heart? and, How long 
can compensation be maintained? Due regard should also 
be had for the presence of associated diseases—diseased 
arteries, heart, and kidneys. 

Treatment. Much can be done to check the course of 
the disease by sending the patient to some warm inland 
place for the winter months at least, where he can lead a 
life out of doors and not contract recurring attacks of bron¬ 
chitis. The general health should be built up in every 
way ; over-use of tobacco and of stimulants is to be inter¬ 
dicted ; starches and sugars should be avoided. 

Attacks of dyspnoea are best controlled by drugs that 
dilate the small arteries—chloral hydrate, iodide of potas¬ 
sium, and nitroglycerin. A good combination is as follows : 


Liq. morph, sulph. (Magendie), 

mj; 

Tinct. belladonnae, 

mhj ,* 

Potassii iodidi, 

gr. vij ; 

Spiritus aetheris comp., 

mxv; 

Aquae, 

3 ss.—M. 


Sig. Such a dose every three or four hours. 

Bronchitis is to be treated on general principles. Should 
the cough be harassing, the fluid extract of chekan, in 
dram doses every three hours, is often of the greatest ser¬ 
vice. The fluid extract, desiccated and given in capsule, is 
a convenient and pleasant form of administration. Ter- 
pin and the turpentine derivatives are of service should 
the expectoration be profuse. 

When the right heart begins to fail and venous conges¬ 
tions appear, cardiac stimulants are indicated. Of these 
strychnine is especially useful. The bowels should be kept 


362 MANUAL OF THE PR A C TICE OF MEDICINE. 

freely open, and all tendency to flatulent dyspepsia is to be 
combated by diet and drugs. Should the venous conges¬ 
tions be urgent and the patient be fairly robust, free bleed¬ 
ing is often followed by marked improvement. 

GANGRENE OF THE LUNG. 

Etiology. —Gangrene of the lung is caused by infection 
by means of the putrefactive bacteria. As these germs are 
so common in inspired air, a condition of impaired lung- 
vitality must be presupposed. The disease is most com¬ 
monly caused by the entrance of organic foreign bodies 
into the bronchi, from food or other bodies being inhaled 
into the trachea, from “ aspiration- ” or “ deglutition-pneu¬ 
monia,’ or from the perforation of the lung by cancer of 
the oesophagus or of the stomach. It may follow cavities, 
bronchiectasis, or fetid bronchitis. It occasionally follows 
embolism or pressure of the branches of the pulmonary or 
the bronchial arteries, and it is one of the rare sequelae of 
lobar pneumonia. Exceptionally it occurs in debilitated 
subjects, especially those with diabetes, without antecedent 
pulmonary disease. 

Pathology.—A circumscribed and a diffuse form are 
recognized. 

The circumscribed form occurs in single or multiple foci, 
usually in the lower lobe near the periphery. The gan¬ 
grenous area is converted to a greenish-brown offensive 
mass surrounded by congested or consolidated lung- 
tissue. The neighboring veins are frequently filled with 
infective thrombi that may become detached, causing sec¬ 
ondary foci in other parts of the body. In this way abscess 
of the brain may be developed. If the pleura be involved, 
pleurisy with a sanious or purulent effusion will result, or 
perforation of the pleura will lead to pyo-pneumothorax. 
Severe and even fatal hemorrhage will result from erosion 




GANGRENE OF THE LUNG. 363 

of a large arterial branch. An intense general bronchitis 
always complicates the disease. Liquefaction of the gan¬ 
grenous area rapidly occurs, and, the softened portions 
being coughed up, a cavity with ragged necrotic walls is 
left. Should the patient recover, a connective-tissue cap¬ 
sule forms, enclosing the cavity, which may subsequently 
contract. 

The diffuse form may be so from the start or may follow 
the circumscribed form. A lobe or the greater part of a 
lobe, or even the entire lung, may thus become gangrenous. 
The diffuse form rarely follows lobar pneumonia. 

Symptoms.— Pulmonary .—There is a cough with an ex¬ 
pectoration which is fetid and usually abundant. On stand¬ 
ing, the expectoration separates into three layers—an upper 
layer, frothy and opaque; a middle layer, clear and watery, 
and usually of a greenish or brownish tinge; and a lower 
layer, of a greenish sediment which consists of mucus, pus, 
shreds of elastic lung-tissue, granular matter, crystals of 
fatty acids, and bacteria. 

Blood is often present in the sputa, and large hemorrhages 
may occur. Marked and characteristic fetor of the breath 
is rarely absent. Pain occurs if there be pleurisy. 

Septic .—There is developed an irregular fever with pros¬ 
tration. The patient loses flesh and strength and passes 
into a typhoid condition. In cases in which the gangrenous 
area is encapsulated the septic symptoms are not so severe 
as one would expect. 

The physical signs are those of consolidation over a cer¬ 
tain area, followed by the signs of a pulmonary cavity. 
There are abundant moist bronchial rales. Physical signs 
of pleurisy with effusion or of pyo-pneumothorax may be 
present. 

The diagnosis from fetid bronchitis is made by finding 
shreds of pulmonary tissue and elastic fibres in the sputum. 


364 MANUAL OF THE PRACTICE OF MEDICINE. 

The prognosis is bad, but not hopeless. The course may 
be acute, or the disease may last for months. 

Treatment consists in supporting the strength of the 
patient and in disinfecting the lung as thoroughly as our 
limited means will permit. The patient should wear con¬ 
tinuously a Robinson inhaler saturated with equal parts of 
alcohol, creosote, and chloroform. Terpin and the deriva¬ 
tives of turpentine are often of great service, while myrtol, 
(gr. iiss in capsule every two hours) is warmly advocated. 

If the gangrenous area be localized near the surface of 
the lung, injections of antiseptics may be made directly 
into it, and if the patient be in fair condition, the cavity 
may be opened through the chest-wall and drained. 

ABSCESS OF THE LUNG. 

Etiology. —Aside from the cases of purulent infiltration 
complicating lobar pneumonia or broncho-pneumonia, ab¬ 
scess of the lung may occur from the following causes 1 

1. From the introduction of foreign septic substances into 
the bronchi, as in aspiration- or deglutition-pneumonia, from 
septic diseases of the throat or the neck, from perforation into 
the lung of cancer of the oesophagus or the stomach or ab¬ 
scess of the liver, or from penetrating wounds of the thorax. 

2. It may complicate lobar pneumonia or phthisis, or it 
may be due to the suppuration of an echinococcus cyst. 

3. More commonly abscess of the lung results from infec¬ 
tive emboli, the so-called “embolic” or “ metastatic abscess.” 
Multiple abscesses frequently occur with pymmia or with 
malignant endocarditis involving the right heart. At first 
the lesion resembles an ordinary hemorrhagic infarction, 
but the embolic area rapidly becomes purulent and softens 
to form a cavity, while the pleura over it becomes infected, 
resulting usually in empyema or pyo-pneumothorax. 

The symptoms are frequently masked by those of the 


SYPHILIS OF THE LUNG. 365 

original disease. Respirations, however, are quickened, the 
temperature becomes higher, and the patient is evidently 
much worse. Pain, if present, is due to the pleurisy. Em¬ 
pyema or pyo-pneumothorax may add its symptoms. The 
sputum is abundant, purulent, and contains shreds of lung- 
tissue. The odor is offensive, but not so markedly so as in 
fetid bronchitis or in gangrene of the lung. The constitu¬ 
tional symptoms are those of sepsis. 

The physical signs at first are those of consolidation, be¬ 
coming changed later to those of a cavity. Complicating 
pleurisy with effusion or pyo-pneumothorax adds its charac¬ 
teristic physical signs. 

The prognosis is almost always fatal in embolic cases, 
but recovery occasionally occurs after pneumonia. Prompt 
and efficient treatment, however, may moderate the mortal¬ 
ity rate. 

The treatment should be entirely surgical, consisting in 
the opening and draining of the abscess-cavity. Recovery 
or improvement results in about one-half the cases so 
treated. 


SYPHILIS OF THE LUNG. 

Syphilis of the lung is a rare disease, but its actual 
occurrence is undoubted. 

Pathology. —Three distinct forms of lung-syphilis are 
recognized : 

1. White Hepatization , or White Pneumonia .—This form 
is seen in stillborn children with other evidences of heredi¬ 
tary syphilis. The lesion consists in the infiltration and 
thickening of the walls of the alveoli, the blood-vessels, 
and the bronchi with small cells. Some of the air-spaces 
are filled with epithelial cells. These cases are of patho¬ 
logical rather than of clinical interest. 

2. Gummata may occur in the lung as a late tertiary 


366 MANUAL OF THE PRACTICE OF MEDICINE. 


manifestation. The gummata are distributed through the 
lungs and are especially numerous at the bases; they vary 
from a microscopical size to that of a lemon. Each gumma 
is usually surrounded by a zone of consolidation. There 
are usually a general bronchitis, thickened pleura, and some 
interstitial pneumonia as complicating lesions. 

Destructive syphilitic processes in the lung have not as 
yet been proved. Cases of gummatous pneumonia re¬ 
semble, clinically, tubercular broncho-pneumonia or new 
growths of the lung. 

3. Syphilitic Fibroid Pneumonia .—In this form the pleura 
is thickened, and bands of connective tissue extend from it 
into the lung. The bronchi are surrounded by a growth of 
connective tissue, which may either so compress them as to 
cause urgent dyspnoea or may weaken them and allow of their 
dilatation. Patches of indurated connective tissue may re¬ 
place the lung-parenchyma, rendering certain portions of the 
lung completely solid. All these lesions are found especially 
well marked at the base of the lung. The physical signs 
are those of bronchitis, bronchiectatic cavities, thickened 
pleura, and areas of consolidation. 

The treatment is that of tertiary syphilis, but it is usually 
ineffective. The course of the disease is slow, and the 
termination is usually fatal. 

NEW GROWTHS OF THE LUNG. 

The most common forms of neoplasms of the lung are 
carcinoma, especially of the epithelial variety, and sarcoma ; 
more rarely are found enchrondroma and osteoma. Primary 
growths are exceedingly rare. 

Primary carcinoma is usually found as a single growth at 
one apex; it may involve other organs by metastasis 
through the medium of the bronchial glands, or it may 
involve the pleura and the chest-wall by direct extension. 


new growths of THE LUNG. 367 

Secondary carcinoma occurs as scattered nodules 
through out both lungs, each nodule being surrounded 
by a zone of congested and consolidated lung-tissue. 
Either a simple or a malignant pleurisy usually compli¬ 
cates the lesion. 

Sarcoma is usually secondary, and both lungs are involved 
by scattered nodules. The sarcoma is usually of the small- 
celled variety. 

Symptoms.— 1. Symptoms due to involvement of the lungs 
depend on the size, number, and position of the malignant 
growths. If the nodules be small and scattered, the patient 
will complain of dyspnoea and of pain in the chest from the 
complicating pleurisy, and will develop a cough. The 
expectoration is either muco-purulent or bloody, or per¬ 
haps dark and mucoid, the so-called “prune-juice” expec¬ 
toration, which is highly suggestive. In other cases the 
expectoration resembles currant-jelly, and this appearance 
is almost pathognomonic. In the expectoration cancer- 
cells may be found. 

2. Large single growths may cause pressure-symptoms. 
Pressure on the bronchi will cause cough, expectoration, 
haemoptysis, and dyspnoea. Pressure on the vena cava 
will cause congestion and oedema of the arm, the neck, 
and the upper portion of the thorax. Pressure on the 
oesophagus will cause dysphagia. Pressure on nerves will 
cause intercostal neuralgia. If the recurrent laryngeal 
nerve be involved, the patient will develop a brassy cough, 
laryngeal voice, and steady or paroxysmal dyspnoea. 

3. Cancerous cachexia will be shown by a waxy pallor, 
loss of strength, slight afternoon fever, and oedema of the 
ankles. 

4. There may be added the symptoms of primary or sec¬ 
ondary growths. 

Physical Signs.—Inspection may reveal distended veins 


368 MANUAL OF THE PRACTICE OF MEDICINE. 

of the upper thorax and the neck or bulging of the chest- 
wall, which may be mistaken for aneurysm, especially as 
the bulging part may yield a slight expansile pulsation or 
an appreciable transmitted expansion. There may be infil¬ 
trated cervical or axillary glands, and the seat of the primary 
growth may be detected. 

Physical signs depend upon the size and position of the 
tumors. 

1. There maybe only the physical signs of a bronchitis 
with those of a dry pleurisy or of an effusion which in some 
cases is hemorrhagic. 

2. Larger nodules give rise to the signs of scattered areas 
of consolidation. 

3. A single large growth will give rise to an area of flat¬ 
ness, with absence of voice and breathing, surrounded by an 
area of dulness, with bronchial voice and breathing. The 
central flat area is usually exquisitely tender on percussion. 

The prognosis is fatal in from six months to two years. 

Treatment is merely palliative, to relieve suffering. In¬ 
jections of the toxic products of the erysipelas coccus may 
be made in sarcomatous cases. 

ECHINOCOCCUS CYSTS OF THE LUNG. 

Small cysts may exist for a considerable time without 
causing symptoms. Large cysts tend to compress the lung 
and lead to secondary inflammatory changes. 

Rupture into a bronchus will allow of the expectoration 
of fragments of the cyst-wall and of the hooklets, estab¬ 
lishing the diagnosis without doubt. 

Rupture into the pleura is not uncommon. Suppuration 
of the cyst may occur, and gangrene of the lung is not 


uncommon. 



TUBERCULAR INFLAMMATIONS IN GENERAL. 369 


(< b) Tubercular Diseases of the Lung. 

TUBERCULAR INFLAMMATIONS IN GENERAL. 

Definition.—Tubercular inflammation, caused by infec¬ 
tion by the tubercle bacillus, is characterized by the pro¬ 
duction of new tissue of low vitality. 

Etiology.—The bacillus tuberculosis, first described in 
1881 by Koch, is now definitely proved to be the actual cause 
of tubercular disease. The bacillus is a short fine rod having 
a length equal to one-half the diameter of a red blood-cell. 
When stained it presents a beady appearance, probably due 
to spore-growth within it. For the methods of staining the 
germ the reader is referred to works on bacteriology. The 
bacilli are found in all tubercular lesions, but they are more 
numerous in the acute forms of disease. They may gain 
access to the blood-vessels or the lymph-vessels, and become 
generally distributed throughout the body. They are thrown 
off in the expectoration of patients suffering from pulmo¬ 
nary tuberculosis in enormous numbers, and this infected 
sputum, when allowed to dry, enters the air as a fine dust, 
which spreads the disease in every direction and infects 
rooms, carpets, and clothing. 

Modes of Infection.-—1. Hereditary or congenital tubercu¬ 
losis is very rare, although undoubted cases have occurred. 

2. Acquired Tuberculosis. — (a) By Inhalation. —Inhalation 
is the most common method of infection, as is proved by 
the fact that 50 per cent, of all autopsies show some degree 
of tubercular disease of the lungs. Cloisters, prisons, asy¬ 
lums, and infected houses show a marked increase of tuber¬ 
cular inhabitants. The expired air, however, of tubercular 
patients is not infective. 

(, b ) By Inoculation. — Local tubercular lesions may result 
from inoculation incurred by handling tuberculous patholog- 
24 


370 MANUAL OF THE PRACTICE OF MEDICINE. 


ical specimens, infected meat and skins, and by wounds 
being inoculated by impure instruments or by tubercular 
dust. Many cases of tuberculosis in children have followed 
the rite of circumcision, during which the wound has been 
sucked by a tuberculous operator. There is no evidence 
that tuberculosis can be conveyed by vaccination with 
humanized virus. 

(V) By the Ingestion of Tuberculous Meat or Milk. —Strik¬ 
ing examples of the infectious properties of the milk of 
tuberculous cows are, unfortunately, only too common, 
many cases of intestinal and mesenteric tuberculosis being 
directly traceable to this cause. Meat of tuberculous ani¬ 
mals is not always infective, and the process of cooking in 
all probability affords an efficient safeguard against this 
method of transmission. 

Conditions Favorable to Infection.— i. Constitutional 
Conditions. — (a) A family history of tuberculosis is present 
in from io to 50 per cent, of cases, according to various 
authors. It is hard to say, however, in any given case, 
whether the child was born with some inherent tissue-weak¬ 
ness predisposing toward tubercular infection—a naturally 
good soil for the growth and development of the bacilli—or 
whether greater risk for accidental infection was run from 
the child living with, kissing, and sleeping with tuberculous 
parents. In either case, however, transmission of the disease 
is more common when the mother is tuberculous. 

(b) Tubercular infection is more common among weakly, 
sickly subjects with deficient chest-expansion. Any depre¬ 
ciation of the general health diminishes the resistance of the 
tissues and favors infection. It is found that rabbits, by 
being allowed to run freely in the woods, may be kept in 
such perfect condition that they cease to be good subjects 
for the experimental inoculation of the bacilli. 

(y) No age is exempt, but in children tuberculosis of the 


TUBERCULAR INFLAMMATIONS IN GENERAL . 371 

bones, the lymphatics, the meninges, and the intestinal tract 
is much more frequent than in adults. 

(d) The negro affords a fertile soil for the growth of the 
bacilli, and tuberculosis among the American Indians is 
especially frequent. 

2. Local Conditions .—Any local weakness or inflammation 
renders the part of the body affected more susceptible to 
tubercular infection. Bronchitis, enlarged bronchial glands, 
and interstitial pneumonia are frequently found as predis¬ 
posing causes of pulmonary tuberculosis, while intestinal 
catarrh produces conditions favorable for the growth of the 
bacilli in the alimentary tract. Local injuries or operations 
may so weaken the tissues as to allow of infection. Thus 
a simple synovitis from injury may become tubercular, or 
pulmonary tuberculosis may follow severe contusions of the 
chest. 

Structure of Tubercle.—The local action of the tubercle 
bacillus upon the tissues results in the proliferation of pre¬ 
existing cells and in the aggregation of leucocytes. To 
this collection of cells the name of “ tubercle ” is given. 

The first step in the formation of tubercle consists in the 
increase in number of the fixed normal cells, especially those 
of the connective tissue and the endothelium of the capillaries. 
These proliferated cells are known as “epithelioid cells.” 
Giant-cells are formed by the increase in protoplasm and in 
the nuclei of a single cell or by the fusion of several cells. 
Giant-cells are found, however, only in cases in which the 
bacilli have a low degree of vitality. 

The next step consists in the emigration from the neigh¬ 
boring blood-vessels of leucocytes which mix with or sur¬ 
round the above-mentioned epithelioid cells. A network or 
reticulum of fibres is found between the cells, probably 
representing the original interstitial tissue stretched apart by 
the increased cellular elements. The reticulum is most 


372 MANUAL OF THE PRACTICE OF MEDICINE . 

marked at the margin of the tubercle. No new blood-vessels 
are formed in the tubercular growth, and pre-existing blood¬ 
vessels are apt to show lesions of an obliterating endartei itis, 
so that the newly-formed tissue has but feeble vitality. 

When these changes have become sufficiently extensive 
the tubercle appears as a grayish point or nodule, to which 
the name “ miliary tubercle ” is given. By the growth and 
approximation of these miliary tubercles laige aieas may 
be involved, forming the so-called diffuse tubercle. 

Histologically, tubercle cannot always be differentiated 
from other infectious tumors, such as those of syphilis 01 
leprosy, or from ordinary granulation-tissue. Tubercle- 
tissue, however, is characterized by its natural tendency 

toward cheesy degeneration. 

Cheesy degeneration, or “ coagulation-necrosis,” is due 
partly to the local action of the bacilli upon the newly- 
formed cells, and partly to the scanty blood-supply of the 
tubercular nodule. At the centre of the nodule the cells 
die, lose their nuclei and their staining properties, and 
become translucent and structureless. This area of degen¬ 
eration presents an opaque, yellowish-white appearance, and 
by the extension and coalescence of these areas the degen¬ 
eration may become exceedingly extensive. Subsequently 
the degenerated area may undergo (i) softening , so as to 
form a cavity or an ulcer, (2) encapsulation , or (3) in it may 
be deposited the salts of lime. 

Spontaneous healing of tubercular nodules may occur in 

two ways: 

1. The nodule may be surrounded by a fibrous capsule; 
its cheesy centre may be converted to a putty-like mass 
which may be infiltrated with the salts of lime ; or it may 
liquefy and be absorbed, leaving only a puckered cicatrix. 

2. There may be a great increase in the fibroid elements 
of the nodules, so that the tubercle becomes firm, hard, and 


TUBERCULAR DISEASES OF THE LUNG. 373 

does not increase in size. This fibroid or sclerotic change is 
more frequently seen in tubercles of the peritoneum. 

Secondary Inflammatory Processes. —Tubercle seldom 
occurs alone in the tissues, but the irritation caused by its 
growth produces secondary inflammatory changes, so that 
the tubercle may become a very composite structure. 

Symptoms of Tubercular Disease. —The action of 
tubercle bacilli is at first entirely local. The affected area 
may be small, and the resulting symptoms consequently 
slight and localized. In other cases the local lesion may 
spread by continuity, so that large portions of important 
organs may be rendered unfit to fulfil their functions, with 
resulting symptoms that are not only local but general. 
In still other cases the lesion is at first localized, but from 
softening and breaking down of a tubercular deposit the 
bacilli may enter a blood-vessel or a lymphatic, enter the 
general circulation, and set up miliary tubercles wherever 
they happen to lodge. The symptoms resulting from such 
a scattering of the lesion are those of an acute infectious 
disease combined with the local symptoms of tuberculosis 
in different parts of the body. This form is spoken of as 
“ acute miliary tuberculosis ; ” it is considered under the 
heading Infectious Diseases. The danger of this general 
infection must always be borne in mind in every tubercular 
inflammation, no matter how localized it may beat the onset. 

TUBERCULAR DISEASES OF THE LUNG. 

Under this heading may be included—1. Acute pulmo¬ 
nary tuberculosis; 2. Chronic pulmonary tuberculosis; 3. 
Acute pulmonary phthisis; 4. Chronic pulmonary phthisis. 

Acute Pulmonary Tuberculosis. 

Etiology. —In this form of disease the bacilli reach the 
lung either through the inspired air or by being transported 


374 MANUAL OF THE PRACTICE OF MEDICINE. 

by the blood. In the latter case tubercular involvement of 
the bronchial glands may precede the pulmonary tuber¬ 
culosis. In other cases some old tubercular process is 
found to be the source of infection. 

Pathology.—Disseminated tubercles are found in part 
of a lung or scattered throughout both lungs. Each miliary 
tubercle is surrounded by a slight zone of congested or 
consolidated air-vesicles, but the greater part of the inter¬ 
vening lung-tissue is comparatively normal, and this condi¬ 
tion sharply defines the disease from pulmonary phthisis, 
in which consolidation of the intervening lung-tissue is an 
early lesion. The tubercles usually are first found at the 
apex of one lung, from which point they may spread; or 
tubercles may be formed at once throughout both lungs in 
great numbers. There is always a catarrhal inflammation 
of the finer bronchi of that portion of the lung occupied by 
the tubercles; in rarer cases the bronchitis is general. 
Tubercles in or near the pulmonary pleura result in pleurisy 
either with fibrin or with serous effusion. As the tubercles 
grow and coalesce, portions of lung may be rendered solid, 
but this consolidation is always a late manifestation of the 
disease. From areas of softening breaking into one another 
small cavities may be formed, and these cavities may be 
still further increased in size by tubercular ulceration of the 
bronchi leading into them. 

Symptoms.— i. Cases in which tubercles are rapidly 
formed throughout both lungs and in other parts of the 
body are really examples of acute miliary tuberculosis; 
they are considered in the discussion of that disease. 

2. The term “ pulmonary tuberculosis ” is applied more 
properly to those cases in which tubercles spread from the 
apex of one lung and are not found in other parts of the 
body—a purely localized process. 

In some cases the disease may develop as a primary 


TUBERCULAR DISEASES OF THE LUNG. 375 

infection, while in other cases it complicates some pre-exist¬ 
ing tubercular lesion. When the disease is established the 
symptoms depend upon the extent of lung involved, the 
bronchitis, and the pleurisy. 

The patient has a fever, higher in the afternoon, followed 
by sweating at night. The heart’s action is rapid. Breath¬ 
ing is rapid and often insufficient, and is made more rapid 
by extension of the tuberculosis or by increase of the bron¬ 
chitis or of the pleurisy. However rapid the breathing, 
there is not apt to be much subjective dyspnoea, even 
though there be marked cyanosis. Cough is a fairly con¬ 
stant symptom, and may be most distressing. The expec¬ 
toration is muco-purulent and may contain blood. In the 
sputa the bacilli are usually, but not invariably, present. 
Loss of flesh and of strength is noted from the first, but it 
seems to bear no direct relation to the extent of lung- 
involved. There is often developed a peculiar pallor of the 
skin, resembling that of pernicious anaemia. In other cases 
the skin is cyanotic. 

In some patients the symptoms progress steadily, ema¬ 
ciation becomes extreme, and death results from exhaustion 
or from secondary involvement of other organs, or the 
patient may pass into a typhoid state. In other cases the 
process will apparently stop for a time, with a general im¬ 
provement of all the symptoms. Once quiescent, the 
tuberculosis may never again extend, and a permanent 
cure may thus be affected. In other cases, after an in¬ 
terval the process will again start up and involve fresh 
areas of the lung, with a return of the old symptoms. In 
still other cases intercurrent attacks of bronchitis, pleu¬ 
risy, or pneumonia occur to modify the course of the 
disease. 

The physical signs may be described as appearing in 
three stages : 


376 MANUAL OF THE PRACTICE OF MEDICINE . 

i. The tubercles are scattered at one apex; there is a 
localized terminal bronchitis and a dry pleurisy. There is 

diminished expansion at the apex. The 
percussion-note may be normal, tym¬ 
panitic, or slightly dull. Vocal fremi¬ 
tus is usually unchanged. Breathing 
sounds may be feeble or harsh and 
puerile, but at this stage no tendency 
toward bronchial breathing is ob¬ 
served. On auscultation crepitant and 
subcrepitant pleuritic rales and fine 
bronchial rales are heard, affording 
strong presumptive proof of pulmo¬ 
nary tuberculosis when localized at 
one apex (Fig. 38). 

2. As the tubercles grow and co¬ 
alesce, portions of lung—usually one 
or both apices—are rendered solid. 
Over these portions the note becomes 
dull, the expiratory sound becomes 
prolonged and high-pitched, and ultimately bronchial breath¬ 
ing and bronchophony are developed. The physical signs 
noted in the preceding paragraph spread at the periphery 
of the lesion (Fig. 39). 

3. When small cavities begin to be formed, gurgles make 
their appearance. The cavities are rarely large enough to 
yield other and more distinctive signs, although a number of 
small cavities may merge into one large antrum over which 
can be obtained a tympanitic or a “cracked-pot” note with 
broncho-cavernous or cavernous breathing (Fig. 40). 

The diagnosis of pulmonary tuberculosis should be sus¬ 
pected in every case of dry pleurisy at the apex or of 
bronchitis at the apex. The disease should be suspected 
in every case of severe recurrent bronchitis or dry pleu- 



Fig. 38.—Physical signs in the 
earliest stage of pulmonary tu¬ 
berculosis : diminished expan¬ 
sion ; percussion normal or 
tympanitic ; breathing weak or 
harsh; pleuritic or bronchial 
rales. 






TUBERCULAR DISEASES OF THE LUNG. 


3 77 


risy, if the constitutional symptoms be out of proportion 
to the apparent lesion. It should be suspected in the case 
of any patient with fever and rapid pulse without apparent 


Fig. 39.—Physical signs of pulmonary 
tuberculosis in the advanced stage : a, di¬ 
minished expansion, dulness, bronchial 
voice and breathing, increased vocal fremi¬ 
tus; pleuritic and bronchial rales; b, dull 
tympanitic note, prolonged and high- 
pitched respiration, bronchial and pleuritic 
rales ; c, tympanitic or normal note, feeble 
or harsh breathing, pleuritic and bronchial 
rales. 

cause, even in the absence of definite pulmonary symptoms. 
The positive diagnosis, however, can only be made by the 
finding of tubercle bacilli in the sputa. 

The prognosis of rapidly-spreading tuberculosis is bad. 
Under proper environment the disease may become chronic 
or may even become quiescent. 

Treatment of all tubercular diseases of the lung will be 
considered later (see p. 395). 

Chronic Pulmonary Tuberculosis. 

Chronic pulmonary tuberculosis differs from the acute 
form in the chronicity of its course and the slow reactive 




Fig. 40.—Physical signs of pulmonary 
tuberculosis in the final stages ; a, signs 
of consolidation, gurgles, and pleuritic 
rales; b, signs of consolidation and rales; 
c, dull tympany, prolonged, high-pitched 
expirations, rales; d, tympany, feeble 
breathing, rales. 









378 MANUAL OF THE PRACTICE OF MEDICINE. 

nature of the secondary inflammatory processes. Three 
distinct clinical groups may be described : 

I. Miliary tubercles are formed at one apex and slowly 
spread downward. The opposite apex is next involved in 
like manner. When the disease is fully developed the 
tubercles are found scattered throughout both lungs. The 
miliary tubercles run a very inactive course, some becoming 
cheesy, while others undergo fibroid change or are encapsu¬ 
lated. There is a chronic bronchitis, at first limited to the 
apex, later becoming general. Bronchiectatic cavities may 
form, but they are of rare occurrence. Dry pleurisy, 
resulting in pleural adhesions and thickening, is due to the 
irritation of tubercles near or in the pulmonary pleura, and 
it is usually best marked at the apex. In the later stages 
of the disease the tubercles may become so closely aggre¬ 
gated as to cause partial or complete consolidation of por¬ 
tions of the lung, especially at the apices; while the forma¬ 
tion of small cavities occurs in the most advanced cases. 

Symptoms begin insidiously. The first complaint may 
be of a hacking cough with scanty expectoration, due, as 
proved by physical examination, to a localized bronchitis at 
one apex. In other cases a dry pleurisy at one apex will 
cause pain to be the initial symptom. Other patients 
suffer from haemoptysis while in apparently robust health. 
In other patients the lesions give no subjective symptoms, 
and the presence of the disease is only discovered by a 
routine examination of the chest. When the disease has 
once developed there is a cough, usually troublesome and 
persistent. It may be dry and hacking or loose in character. 
Expectoration is scanty at first, but later becomes profuse, 
muco-purulent, contains bacilli, and frequently is tinged 
with blood. Haemoptyses may occur from time to time, 
but they are rarely profuse during the early stages of the 
disease. ■ 


TUBERCULAR DISEASES OF THE LUNG. 


379 


Dyspnoea is present according to the extent of lung in¬ 
volved, the bronchitis, and the pleurisy. At first noticed 
only on exertion, it may subsequently become steady and 
distressing. Extension of the pleurisy is marked by fever 
and pain. Rapid pulse is almost constant throughout the 
disease, so that pulmonary tuberculosis should be suspected 
in all patients whose pulse is continually rapid without 
apparent cause. Increased rapidity of the pulse and some 
afternoon rise in fever are caused by fresh accessions of 
tubercles or by exacerbations of the pleurisy or the bron¬ 
chitis. 

The patient loses flesh and strength, becomes anaemic, 
and is converted to a semi-invalid. Later in the disease, 
when small cavities form, “ hectic ” develops—the afternoon 
fever, bright eyes, flushed cheeks, night-sweats, and more 
rapid emaciation. 

The physical signs of chronic pulmonary tuberculosis 
resemble those of the acute form. There may at first be no 
physical signs, or there may be diminished expansion, tym¬ 
pany or tympanitic dulness, with feeble or harsh breathing 
at an apex. Auscultation reveals pleuritic and bronchial 
moist rales. In other cases thickened pleura at an apex 
yields dulness and diminished voice and breathing. Later 
appear the signs of partial or complete consolidation— 
dulness, bronchial voice and breathing, and increased vocal 
fremitus with a persistence of the bronchial and pleuritic 
rales. The final stage of small cavities is accompanied by 
gurgles, more rarely by tympanitic or “ cracked-pot ” per¬ 
cussion-note and by broncho-cavernous or cavernous voice 
and breathing. 

Course of the Disease. — (a) In some patients the lesion 
begins at one apex, but after a certain time does not pro¬ 
gress, and the patient lives for years without further trouble. 
The tubercles still remain in the apex of the lung, but they 


380 MANUAL OF THE PRACTICE OF MEDICINE. 


become encapsulated, fibroid, or calcareous. Many of these 
patients suffer so little from their disease that no suspicion 
of tuberculosis is entertained. There is always danger that 
at any time the process will start anew or be the cause of 
an acute general miliary tuberculosis. 

(b) In other patients the lesion is progressive only at long 
intervals. Exacerbations of the lesion are most apt to 
occur during the winter months, during any intercurrent 
pulmonary disease, or whenever the general health is 
allowed to deteriorate. Many old cases of tuberculosis are 
thus stirred into renewed activity by epidemics of the 
“ grippe.” So a great many patients go on for years, each 
succeeding exacerbation becoming more and more severe, 
until finally the extension-process becomes continuous. 
Under proper environment, however, the course even of 
these patients may be prolonged and the progress of the 
disease may ultimately be checked. 

(c) In other patients the course of the disease is continu¬ 
ous. Pulmonary and hectic symptoms become increasingly 
pronounced, and death finally results from emaciation, from 
acute general miliary tuberculosis, from hemorrhage, or 
from secondary tubercular inflammations of the larynx, the 
intestines, or the peritoneum. 

II. Before the time of the tubercular infection the patient 
has suffered from emphysema and chronic bronchitis, possi¬ 
bly with the addition of thickened and adherent pleurae. 
Such a complex pulmonary condition seems to afford a 
fertile soil for the development of the tubercle bacilli, and 
the lesions of pulmonary tuberculosis become combined, 
with the pre-existing morbid changes. The patient at first 
complains only of the symptoms of the original disorders, 
but is evidently more seriously sick than he should be with 
emphysema and bronchitis alone. Gradually the more char¬ 
acteristic symptoms of tuberculosis appear, and the regular 


TUBERCULAR DISEASES OF THE LUNG. 381 

physical signs are obtained. The course of this set of 
clinical cases resembles that of the first variety, but is much 
more serious, and recovery can hardly be expected. 

III. The third set of cases resembles either of the pre¬ 
ceding forms except that there is added an interstitial 
pneumonia. The connective tissue may be arranged around 
the tubercles, along the bronchi, may extend inward from 
the pleura in broad bands, or may occur diffusely, ren¬ 
dering parts of the lung completely solid and fibrous. As 
the result of the interstitial pneumonia the walls of the 
bronchi become weakened and bronchiectatic cavities are 
permitted. By suppuration or tubercular ulceration of the 
walls of the dilated bronchi the bronchiectatic cavities are 
still further increased in size. The interstitial pneumonia 
may precede or follow the deposit of tubercles in the lung. 

The symptoms are more severe than those of the two 
previous forms, resembling those of chronic pulmonary 
phthisis. The bronchitis, however, is more extensive; the 
expectoration is more abundant and may be significant of 
bronchial dilatation; the dyspnoea is more distressing. 
Hectic is present in the majority of cases, and repeated 
small haemoptyses may occur from the suppurating or 
ulcerating mucous membrane lining the bronchiectatic 
cavities. If the interstitial tissue be abundant there will be 
offered resistance to the flow of blood through the lungs, 
with hypertrophy of the right ventricle and the symptoms 
of its dilatation in the latter stages of this disease. To this 
form of “ pulmonary tuberculosis ” the term “ fibroid 
phthisis ” is often applied. 

The prognosis of pulmonary tuberculosis is generally 
better than that of phthisis. The association of emphy¬ 
sema or of interstitial pneumonia with the deposition of 
tubercles renders the prognosis more serious than that of 
uncomplicated tuberculosis, not only because the lung is 


382 MANUAL OF THE PRACTICE OF MEDICINE. 

further disabled, but because of the additional danger of 
failure and dilatation of the right ventricle. 

The treatment of all tubercular inflammations of the 
lung will be considered later (see P- 395 )■ 

Acute Pulmonary Phthisis. 

Synonyms.—Acute consumption ; Galloping consump¬ 
tion ; Phthisis florida. 

Acute pulmonary phthisis is a much more complex dis¬ 
ease than tuberculosis, because other inflammatory changes 
are mixed with the tubercular lesions in the lungs. Tuber¬ 
culosis means tubercles alone; phthisis means tuberculosis 
plus lobar pneumonia or broncho-pneumonia. 

Etiology.—Phthisis may be a primary disease or may 
follow some previous tubercular inflammation of the lung. 
A person predisposed to tuberculosis will develop phthisis 
when exposed to the cause of inflammation of the lung 
with infection at the same time by the tubercle bacilli. 

Pathology.—The process usually starts at the apex of 
one lung and involves the lobe or even the entire lung. In 
other cases the process may be more evenly distributed 
throughout both lungs. The affected portions of the lung 
are consolidated from gray or red hepatization or from 
yellowish nodules. There are frequently cavities. The 
bronchi are inflamed and bronchiectasis may occur. There 
is fibrin in the pulmonary pleura. 

It seems better to describe separately (1) the yellowish 
nodules, (2) the pneumonia, (3) the lesions in the bronchi, 
and (4) the cavities. 

1. The yellowish nodules vary in size from that of the 
head of a pin to that of a goose-egg. By the coalescence 
of these nodules still larger nodules may be formed. These 
nodules consist of tubercle-tissue in the condition of coagu¬ 
lation-necrosis. The tubercle-tissue may fill the air-spaces 


TUBERCULAR DISEASES OF THE LUNG. Plate 21. 




S' 




V 

O 






l 


1 




( ' 



\ 




% 




s 




1 ubercle bacilli in the sputum, fiist colored with anilin-fuchsin and then w ith methylene 

blue; x about 1000 (Vierordt). 






TUBERCULAR DISEASES OE THE LUNG. 383 

and the small bronchi, being grouped like the inflammatory 
products of lobar pneumonia; or it may be grouped in the 
air-vesicles around a bronchus whose wall is infiltrated with 
tubercle-tissue, in this case resembling the grouping of the 
inflammatory products of broncho-pneumonia. These 
nodules are practically composed of dead tissue, and can 
never be recovered irom. They may undergo softening 
and form large cavities. 

2. The pneumonia surrounds the nodules and involves 
the lung-tissue between them. The hepatization may be 
red or gray in color. In some cases the pneumonia prod¬ 
ucts fill the air-vesicles of a lobe or of the greater part of a 
lobe, resembling lobar pneumonia. In other cases the 
grouping is that of a broncho-pneumonia : the pneumonic 
products occur in patches, each one of which consists of 
a bronchus with infiltrated walls surrounded by a zone of 
consolidated air-cells. By the possible coalescence of these 
peribronchitic patches large areas of lung are rendered solid. 
The products of either form of pneumonia are perfectly 
capable of resolution, so that the lung can again return to a 
healthy condition. 

3. The bronchi may be the seat of a catarrhal inflam¬ 
mation, or their walls may be infiltrated by the products 
of tubercular or non-tubercular inflammation. Infiltration 
of the bronchial wall weakens it, allowing of cylindrical 
or sacculated dilatation. If the infiltration be tubercular, 
ulceration of the bronchial wall may occur, still further 
increasing the size of the bronchiectatic cavity. 

4. Cavities may be formed in several ways: (a) By the 
breaking down of tubercular nodules; {b) by bronchial 
dilatation ; ( c ) by ulceration of the walls of the bronchi. 

Grouping of the Lesions .—Delafield describes three dis¬ 
tinct types of phthisis, having the same clinical history, but 
differing in appearance and in the physical signs: 


384 MANUAL OF THE PRACTICE OF MEDICINE . 

1. One or more lobes are completely consolidated by the 
filling of the air-spaces and the small bronchi with epithe¬ 
lium, fibrin, and pus. Scattered throughout the consolida¬ 
tion are tubercular nodules. The pleura is coated with 
fibrin. This form of phthisis is described as “acute pneu¬ 
monic phthisis” or “acute tubercular pneumonia.” 

2. There is a general catarrhal bronchitis, and a tuber¬ 
cular inflammation of the walls of some of the bronchi and of 
small zones of air-spaces surrounding them. This form of 
phthisis is spoken of as “ tubercular broncho-pneumonia. 

3. The third type resembles the preceding form except 
that in addition to the tubercular broncho-pneumonia there 
are larp^e or small areas of diffused consolidation due to 

o 

the filling of the air-spaces with fibrin, pus, and epithelium. 

Cavities and bronchiectasis may occur in any one of the 
preceding types. 

The symptoms of phthisis begin acutely or gradually. 
If the onset be sudden , the symptoms resemble those of 
pneumonia. There is a chill followed by fever, pain in the 
side, a cough with mucous or muco-purulent expectoration, 
and much prostration. 

The differential diagnosis of these cases from pneumonia 
is always difficult, and during the first days of the disease 
it may be absolutely impossible. Pneumonia, however, 
defervesces between the sixth and the twelfth day, with im¬ 
provement of all symptoms, whereas in phthisis the patient’s 
condition becomes aggravated, night-sweats appear, and 
the expectoration is more purulent and profuse. Even 
then the case may resemble one of tardy resolution. In 
pneumonia haemoptysis does not occur; in phthisis it may 
be an early symptom. The fever in phthisis is more remit¬ 
tent than in pneumonia. Should cavities form or bacilli be 
found in the sputum, the differential diagnosis would present 
no difficulties. 


TUBERCULAR DISEASES OF THE LUNG. 385 

If the onset be gradual , there will be a cough, dry at 
first, later becoming moist and accompanied by a muco¬ 
purulent expectoration which may contain blood. Haemop¬ 
tysis in considerable amounts may occur. There is a fever 
of from ioo° to 102° F. with afternoon exacerbations. The 
breathing is rapid, but subjective dyspnoea is seldom dis¬ 
tressing. When the disease is developed the cough becomes 
looser; the expectoration becomes more abundant and 
more purulent and contains the bacilli. Large haemoptyses 
arise from ulcerated arterial branches in the walls of 
cavities; repeated small hemorrhages arise from the ulcer¬ 
ating walls of bronchiectatic cavities. 

The fever is usually remittent—about ioo° F. in the 
morning, with an afternoon exacerbation to 103° or 104° F. 
The remissions occur regularly in the early morning hours; 
they are accompanied by profuse cold sweats, especially 
about the head and the neck. During the exacerbation of 
the fever the cheeks are flushed, the eyes are bright, and 
the whole demeanor of the patient is cheerful throughout. 
The pulse becomes increasingly rapid and feeble; the 
breathing becomes more and more rapid, and it may be so 
inefficient that cyanosis becomes marked, but there is rarely 
any complaint of dyspnoea. The patient rapidly loses flesh 
and strength and becomes anaemic. 

The physical signs at first are those of broncho-pneu¬ 
monia or of lobar pneumonia. Over the consolidated por¬ 
tions of the lung there are diminished expansion, dulness 
on percussion, bronchial breathing with bronchophony, and 
subcrepitant and crepitant rales. If there be a tubercular 
broncho-pneumonia without much consolidation, there may 
be only sibilant and sonorous breathing with bronchial rales, 
or small areas over which there are dulness on percussion, 
intensified voice, and crepitant and subcrepitant rales. 
When cavities form there is obtained tympanitic dulness 
25 


386 MANUAL OF THE PRACTICE OF MEDICINE. 

or a “ cracked-pot ” or even an amphoric note ; the breath¬ 
ing and the voice become cavernous, and gurgles and churn¬ 
ing rales make their appearance. In cases in which the 
cavities are full of secretion there may be flatness and 
absence of voice and breathing, but moist rales of all kinds 
are heard with both inspiration and expiration. 

Course of the Disease.—(i) Some patients die in two 
or three weeks in a typhoid condition or from exhaustion or 
hemorrhage. The diagnosis of lobar pneumonia is often 
made in these cases. (2) In other patients the disease is 
prolonged for several months. (3) Some patients pass into 
the condition of chronic phthisis. (4) In a small minority 
recovery may occur; the tubercular products are encapsulated 
or undergo fibroid change, while the non-tubercular prod¬ 
ucts undergo resolution. 

The prognosis of acute phthisis is unfavorable. Recovery 
is rare, but in a large number of patients the lesions become 
chronic, so that life may be considerably prolonged. 

The treatment of acute cases resembles that of pneu¬ 
monia; in subacute cases the treatment is that of chronic 
pulmonary phthisis. 

Chronic Pulmonary Phthisis. 

Etiology and Synonyms.—Chronic phthisis may appear 
as a primary form of disease or may be secondary to pulmo¬ 
nary tuberculosis or to any pre-existing tubercular disease 
of the lung. The chronic form may follow acute phthisis or 
may be chronic from the start. Synonyms: Chronic con¬ 
sumption ; Chronic ulcerative phthisis. 

Pathology.—The lesions of chronic phthisis resemble 
those of the acute form, except that they are modified by 
their long duration and that there is added an interstitial 
pneumonia. Separate descriptions may be given of (1) the 
tubercular nodules, (2) the pneumonia, (3) the interstitial 


TUBERCULAR DISEASES OE THE LUNG. 387 

pneumonia, (4) the changes in the bronchi, (5) the cavities, 
and (6) the lesions in the pleura. 

1. The tubercular nodules are arranged as are those of 
acute phthisis. In some cases the air-spaces are filled with 
tubercle-tissue; in other cases peribronchitic areas of tuber¬ 
cular consolidation occur, the wall of the central bronchus 
being infiltrated with tubercle-tissue. The tubercular 
nodules may undergo coagulation-necrosis or may break 
down, forming cavities. In favorable cases the nodules 
undergo fibroid change or become encapsulated with cheesy 
or calcareous centres. 

2. The products of pneumonia are grouped like those of 
the lobar form, the air-spaces being filled with fibrin, pus, 
and epithelium, or there may be the peribronchial nodules 
of a broncho-pneumonia. 

3. The interstitial pneumonia develops in several ways: 
(a) There may be areas of lung-tissue converted more or 
less completely to fibrous masses. The walls of the air¬ 
spaces are thickened ; their cavities are encroached upon 
by polypoid outgrowths of connective tissue, and they may 
be filled with epithelial cells, (b) Bands of connective 
tissue extend along the bronchi, the blood-vessels, and the 
septa between the lobules, (c) Bands of connective tissue 
penetrate the lung, extending inward from a thickened and 
adherent pleura. 

4. The bronchi undergo the same inflammatory changes 
as in acute phthisis : (a) They are the seat of a chronic 
catarrhal inflammation, (b) Their walls may be infiltrated 
by the products of a tubercular or a non-tubercular in¬ 
flammation, and, being thus weakened, sacculated bron¬ 
chial dilatation will result. ( c ) If the infiltration be tuber¬ 
cular, ulceration of the bronchial wall will further increase 
the size of the bronchiectatic cavity. 

5. Cavities are formed— (ci) By the softening and break- 


388 MANUAL OF THE PRACTICE OF MEDICINE. 

ing down of areas of coagulation-necrosis; ( b ) by bronchi¬ 
ectasis ; and (c) by tubercular ulceration of the walls of the 
bronchi. Cavities, when once formed, tend to enlarge, and 
as they increase in size they touch and open into one an¬ 
other. In this way the greater part of a lobe may be con¬ 
verted to a single large cavity. A blood-vessel is the last 
structure to be ulcerated in the formation of a cavity. An 
obliterating endarteritis usually occurs, converting the ves¬ 
sel to a fibrous cord, thus preventing hemorrhage at the 
time of its erosion. Should this conservative process not 
be completed, partial erosion of the arterial wall will allow 
of the formation of a little aneurysm, which may finally rup¬ 
ture, causing profuse hemorrhage. Conservative and heal¬ 
ing processes may occur even after a cavity has once formed. 
The wall of the cavity becomes thick and fibrous, and the 
lining may be smooth, resembling mucous membrane. 
Healing processes, however, do not occur in cavities of 
any size. 

6 . The pleura over the involved area of lung is regularly 
the seat of a chronic inflammation, resulting in thickening 
and adhesions. This form of chronic inflammation is really 
conservative, as, by the strengthening of the pleura by con¬ 
nective tissue the risk of perforation of cavities or of bacte¬ 
rial infection of the pleura is minimized. 

The lesions of chronic phthisis usually begin at the apex 
of one lung and extend downward to involve the upper lobe 
and the apex of the lower lobe. The opposite apex is then 
regularly affected. 

Complicating and secondary lesions will be considered 
under the heading “ Complications.” 

Symptoms.—The mode of onset is varied and insidious. 

I. The disease may begin with dyspeptic and anaemic 
symptoms not readily alleviated by treatment. Amenor- 
rhoea is an early symptom of these anaemic patients. 


TUBERCULAR DISEASES OF THE LUNG. 389 


2. There may be a gradual loss of flesh and of strength, 
with a slight afternoon rise in temperature. 

3. The symptoms of a “ neglected cold ” may precede 
other symptoms. Cases of recurring or of persistent bron¬ 
chitis, especially in a young person, should always be re¬ 
garded with suspicion. 

4. Chills and fever due to tubercular infection may be 
mistaken for those of malarial origin. 

5. The disease may begin with a laryngeal cough and 
huskiness of the voice, and on examination either a ca¬ 
tarrhal or a tubercular laryngitis may be found, or the 
larynx may appear simply anaemic. 

6. Haemoptysis may be the initial symptom, preceding 
other manifestations of the disease by months or even by 
years. 

7. There may be dry pleurisy, especially at an apex or in 
the scapular region, or a pleurisy with effusion running an 
acute or an insidious course. According to Bowditch, 
phthisis ultimately develops in one-third of the cases of 
pleurisy with effusion. A double pleurisy with effusion is 
much more suggestive of tubercular origin. 

Symptoms of the Developed Disease .— 1. Pulmonary Symp¬ 
toms. — (a) Cough is an early and almost a constant symp¬ 
tom. Dry and hacking at first, it later becomes looser and 
more frequent. It may be so distressing as to prevent sleep, 
and sufficiently severe and paroxysmal to provoke vomiting 
and thus to interfere with the patient’s nutrition, (h) The 
sputum varies in amount and character in the different stages 
of the disease. At first the expectoration is mucous and 
of a glairy consistency, presenting nothing suggestive of 
tubercular trouble. Later in the disease the sputum becomes 
muco-purulent and contains little grayish or grayish-green 
lumps. When cavities form the expectoration is more pro¬ 
fuse, especially in the morning or after sleep, is more puru- 


390 MANUAL OF THE PRACTICE OF MEDICINE. 

lent, and finally the sputa assume the nummular form of 
separate solid purulent masses which sink in water. The 
expectoration of phthisical patients has usually a heavy 
sweetish odor, although it may be fetid. In cases of con¬ 
solidation without much bronchitis the sputum may not be 
abundant at any time. Generally the quantity of the spu¬ 
tum gives a fair test of the activity of the disease. Exam¬ 
ination of the sputum for tubercle bacilli should always 
be made in doubtful cases. The bacilli are usually present 
early in the disease ; they are abundant in proportion to 
the intensity of the tubercular process. A diminished number 
of bacilli affords grounds for a more favorable prognosis. 
The presence of bacilli in the sputum is an infallible proof 
of the existence of tuberculosis, but their absence does not 
necessarily exclude the disease. Tuberculosis can be ex¬ 
cluded only after repeated examinations of the sputa show 
absence of the bacilli. 

The demonstration of elastic fibres in the expectoration 
only proves the existence of some destructive pulmonary 
lesion, the fibres being found in tuberculosis, gangrene, and 
abscess of the lung. If the sputum be pressed between 
two thin cover-glasses and held against a black ground, the 
elastic fibres can usually be recognized with the naked eye. 
From the appearance of the elastic fibres it can be told 
whether they are derived from the bronchi, the alveoli, or 
the blood-vessels. 

Hemorrhage occurs in 60 per cent, of all cases of chronic 
pulmonary phthisis; it may appear early or late in the dis¬ 
ease. Large early hemorrhages never lead to phthisis, as 
is erroneously supposed, but arise from a small undiscovered 
lesion. The small early hemorrhages usually arise from 
the congested or ulcerated walls of the bronchi, and the 
blood is admixed with sputum. Large late hemorrhages arise 
from the erosion of an artery or from a ruptured aneurysm 


TUBERCULAR DISEASES Of THE LUNG. 


39 * 


of an artery within a cavity; in these cases the blood is pro¬ 
fuse and is unmixed with sputum. For the differential diag¬ 
nosis of haemoptysis from haematemesis see Pulmonary 
Hemorrhage. 

Small hemorrhages from congested bronchi may relieve 
congestion and may be followed by a feeling of general im¬ 
provement. Large hemorrhages are often fatal, either from 
the exhaustion and anaemia induced by them, or by reason 
of the hemorrhage itself, or because blood is aspirated into 
the bronchi of the other lung, causing asphyxia or septic 
pneumonia. 

Pain may be a distressing symptom or it may be absent 
entirely. When present it is due either to the pleurisy, to 
the muscular strain of coughing, or to intercurrent intercostal 
neuralgia. 

Tenderness is often elicited by percussing over the locality 
of a dry pleurisy. 

Dyspnoea on exertion increases with the extension of the 
disease and with the exacerbations of the bronchitis. Con¬ 
stant dyspnoea usually indicates excessive involvement of 
both lungs or points to some pleural complication. Extreme 
dyspnoea with cyanosis is practically unknown in uncom¬ 
plicated cases. Pain and sudden urgent dyspnoea suggest 
pneumothorax. 

Constitutional Symptoms .—Fever usually is marked in 
proportion with the advance of the lesion, and a persistently 
normal temperature usually means that the disease is not 
progressing. It is possible, however, for consolidation alone 
to cause no fever, the febrile condition in general being due 
to the bronchitis and to the suppuration in the cavities. 
The fever is usually remittent or even intermittent, the 
minimum temperature occurring between 2 and 6 o’clock 
A. m ., the maximum being noted between 2 and 6 o’clock 
p. m. The afternoon rise of temperature is usually accom- 


392 MANUAL OF THE PRACTICE OF MEDICINE. 

panied with flushed face, brilliant eyes, and a “ hectic flush.” 
The early morning remission is marked by profuse cold 
night-sweats, especially about the head and the neck. The 
sweating in advanced cases also recurs during the day, after 
sleeping. When extensive suppurating cavities exist the 
morning temperature may be subnormal. A continuous 
high temperature suggests an intercurrent pneumonia. The 
temperature is often influenced by rest and by good nurs¬ 
ing, and usually declines with hospital care. The tempera¬ 
ture becomes also less marked under favorable changes of 
climate. 

The pulse is rapid, full, and compressible, and there may 
be capillary pulsation visible under the finger-nails. 

The patient loses flesh and strength and becomes anaemic. 
These changes depend upon the fever, the progress of the 
disease, and the proper feeding and treatment of the patient. 
The weight, which gives a good index of the progress of 
the disease, should always be considered in the prognosis. 
It is possible, however, for the patient to retain flesh, 
strength, and color even with a well-advanced lesion. 

The mental state is peculiarly cheerful, and even mori¬ 
bund patients are firmly confident of a speedy recovery. 

Menstruation in women becomes irregular or ceases 
altogether. 

Digestive Symptoms.—Anorexia may be a well-marked 
symptom, so that there is actual loathing for all food. 
Nausea and vomiting may appear in the later stages, being 
due to paroxysms of coughing or to dilatation or a chronic 
catarrhal inflammation of the stomach. As a rule, how¬ 
ever, phthisical patients digest well, although the stomach 
lacks its normal peristaltic power and the gastric juice is 
deficient in HC 1 . 

Diarrhoea often appears in the later stages of the disease; 
it may be due to waxy or fatty degeneration of the liver, to 


TUBERCULAR DISEASES OF THE LUNG. 393 

catarrhal enteritis, to amyloid degeneration, or to tubercular 
ulcerations of the intestine, especially of the large bowel. 
Tubercular ulceration of the ileum may cause no diarrhoea, 
but it induces an emaciation that cannot otherwise be 
accounted for. In some cases no lesion is found post¬ 
mortem to account for the diarrhoea. 

Physical Signs.— 1. Signs of Early Cases .—There is 
usually appreciated by palpation a diminished respiratory 
expansion at one apex; this sign, which often precedes 
all other physical signs, is of great diagnostic importance. 
The percussion-note over and under the clavicle may be 
normal or slightly dull. Breathing (1) may be simply 
feeble, or (2) the inspiration may be inaudible, while the 
expiration is unduly prolonged, or (3) the respiratory 
murmur may be harsh and rude and of the peculiar wavy, 
jerky character spoken of as “ cog-wheel ” breathing. Fine 
moist bronchial rales and subcrepitant pleuritic rales are fre¬ 
quently heard even in early cases. 

2. Signs of Evident Consolidation .—The deficiency of 
local chest-expansion becomes more marked, and inspection 
may show some sinking of the infraclavicular spaces. The 
percussion-note is slightly dull; the breathing and the voice 
approach the broncho-vesicular (louder and higher piched 
than normal, with an expiration longer and higher in pitch 
than inspiration). Vocal fremitus is usually increased 
unless there be thickened pleura. These physical signs are 
distinctive when obtained at the left apex, but are nearly 
the signs normally obtained at the right apex; the pres¬ 
ence of bronchial and pleuritic rales, however, not being 
normal to either apex, may make the diagnosis evident. 
Later, when consolidation becomes more marked, the dul- 
ness becomes more pronounced, the breathing and the 
voice become bronchial, vocal fremitus is increased, and 
the bronchial rales become coarser and more numerous. 


394 manual of the practice of medicine. 

3. Signs of Cavities .—Numerous scattered cavities with¬ 
out much surrounding consolidation and without pleuritic 
thickening may yield a nearly normal percussion-note. On 
auscultation, however, bronchial breathing and gurgles are 
heard. Small cavities filled with secretion may give rise to 
marked dulness or even flatness. Tympany is excited over 
cavities of about the size of an English walnut. The tympan¬ 
itic quality is best marked when the patient’s mouth is open, 
constituting “ Wintrich’s sign.” A “cracked-pot” note is 
obtained by firm, sharp percussion over superficial cavities 
having yielding walls, with open communication with a 
bronchus. This note often comes and goes, is reproduced 
by coughing, and is best heard when the percussor’s ear is 
placed directly in front of the open mouth of the patient. 
It must be remembered that a “ cracked-pot” note may be 
normally heard at the right apex in some children. An 
amphoric note is heard by percussing large cavities with 
smooth rigid walls. 

The breathing over cavities may be bronchial, broncho- 
cavernous, or cavernous. The breathing signs, however, 
change their character according to whether the cavity is 
empty or is filled by secretion. A distinctive form of breath¬ 
ing heard over cavities consists of a respiratory murmur, 
beginning as vesicular and suddenly breaking into bron¬ 
chial. 

Gurgles and churning sounds are heard over most 
cavities, but there are exceptions in which the cavities are 
dry. 

It should never be forgotten that the signs of a cavity 
may be simulated exactly by a patch of consolidation over 
a large bronchus, so that the diagnosis of a cavity should 
always be made with extreme caution. 

Complications.—There may be pleurisy with effusion or 
empyema. Perforation of the pleura over a softening tuber- 


TUBERCULAR DISEASES OF THE LUNC. 395 

cular nodule results in pneumothorax or of pyo-pneumo- 
thorax. There may be tubercular inflammation of other 
organs, especially meningitis, tubercular laryngitis, and 
ulcerations of the intestine. The kidneys may be tuber¬ 
cular or may be the seat of amyloid change. Chronic 
diffuse nephritis may develop. The liver may be waxy, 
fatty, or the seat of tubercular deposits. Tubercular peri¬ 
tonitis may be present, or septic peritonitis may result from 
the rupture of tubercular intestinal ulcerations. Phthisis at 
any time may be complicated by pulmonary tuberculosis or 
by acute general miliary tuberculosis. Lobar pneumonia is 
not uncommon as a terminal event. There may be developed 
in phthisical patients a form of insanity resembling that 
occurring during the convalescence from acute diseases. 
Peripheral neuritis is occasionally observed. 

The prognosis is grave, but not hopeless. Favorable 
results are common in early cases properly treated by change 
of climate, while spontaneous cures are not infrequent, even 
under unfavorable hygienic surroundings. The prognosis 
is dependent upon the constitutional vigor and the finan¬ 
cial condition of the patient, and the rapidity of growth 
and the extent of the lesions. Repeated haemoptyses are 
unfavorable. 

Treatment of Tuberculosis in General. 

There are three indications for treatment: (1) To prevent 
the spread of the disease; (2) to arrest the disease; and 
(3) to relieve symptoms. 

I. Prophylactic Treatment. — (a) For the General Public .— 
The sputa of all tubercular cases should be collected and 
destroyed. The patient should be warned not to spit about 
the house or in the street. Portable spit-cups are invented 
for the collection of the sputa; or handkerchiefs may be 
used for the purpose if they are thoroughly boiled, after use, 


396 MANUAL OF THE PRACTICE OF MEDICINE. 

in a receptacle separate from that for the other clothes. A 
phthisical patient should sleep alone, and separate state¬ 
rooms on steamships should be provided for tubercular 
cases. Rooms infected by tubercular sputa should be 
disinfected thoroughly before they are again occupied. 
There should be governmental inspection of dairies and 
slaughter-houses, and tuberculosis in animals should be 
stamped out by killing the infected animals. 

Patients with tuberculosis should not marry. In women 
with a suspected tubercular tendency the risk of develop¬ 
ing the disease is largely increased by childbearing. 

(< b) For the Individual .—A child born of tuberculous 
parents should receive careful prophylactic treatment. The 
mother of a tuberculous child should not nurse it nor sleep 
in the same room with it. The child should enjoy the 
recreations of an outdoor life, and studious habits, especially 
in crowded schools, should be sacrificed for athletic pur¬ 
suits. Sedentary occupations are undesirable. Nasal ob¬ 
struction, enlarged tonsils, and adenoid disease, if present, 
should receive prompt attention, so as to allow of the fullest 
extent of breathing. All intercurrent diseases are to receive 
more than usual attention, and the general health is to be 
kept at the highest pitch by fresh air, sufficient sleep, proper 
food, and tonics whenever they may be required. 

2. To arrest the disease two things are necessary—to keep 
the general health good, and to prevent complicating inflam¬ 
mations. These conditions are complied with by (a) climate, 
( b ) hygiene, (r) diet, and ( d ) drugs. 

[a) Suitable change of climate affords the best chance for 
permanent recovery. Usually, however, the change is in¬ 
sisted on too late, and hopeless, even dying, patients are 
sent on long journeys away from friends and home com¬ 
forts. There is no one climate suitable for all tuberculous 
patients, and in the selection of a climate good judgment 


TUBERCULAR DISEASES OF THE LUNG . 397 

and common sense must be employed. Generally speak¬ 
ing, the requirements are a pure atmosphere, an equable 
temperature, and a maximum of temperature. As to the 
exact choice, much depends upon the patient. Young and 
robust patients with early lesions do best usually in a cold, 
bracing climate, where they can lead an active outdoor life 
and become strong and muscular. Such cases do well in 
the Adirondacks or in Colorado. Those who are unable to 
take physical exercise by reason of age, sex, or advanced 
pulmonary lesions do best in a warm, dry, equable climate, 
where they can sit outdoors and keep from catching cold 
without being obliged to exercise. Such a climate is to be 
found in Southern California, North and South Carolina, 
Georgia, Florida, Mexico, Egypt, and Algeria. The more 
unable such patients are to exercise, the warmer the climate 
they seem to need. Some patients are rendered worse in 
the cool climates and are debilitated by warm air. Such 
patients should travel from place to place until they find a 
climate in which they improve in one or two weeks. Other 
patients seem to do best by a variety of climates, and they 
improve by continually travelling. 

(Ii) Hygiene .—Tubercular cases require a maximum of 
fresh air and sunshine. The sleeping-room should be airy 
and sunny. Exercise in the open air should be graded to 
the strength of each patient, much harm being done by con¬ 
scientious exercise past the point of moderate fatigue. The 
skin should be kept open by skin-frictions and daily baths. 
The patient should avoid exposure to inclement weather, 
but over-coddling weakens him and increases his liability 
to catch cold. The patient should wear flannels through¬ 
out the year, but should not be over-clothed, as the danger 
of catching cold is thereby increased. 

(, c ) The diet should be simple, wholesome, and abundant. 
The rule is that tubercular cases should be over-fed. In 


398 MANUAL OF THE PRACTICE OF MEDICINE . 

addition to the ordinary diet, as much milk and cream as 
possible should be taken, and all dyspeptic symptoms 
should receive proper attention. If milk and cream are not 
well borne, cod-liver oil should be given in as large doses 
as the patient will tolerate. Superalimentation by the 
stomach-tube is often of great benefit. Alcohol with meals 
may be allowed if it agrees. 

(d) Drugs .—A large number of specifics are lauded every 
year, but each one fails in fulfilling expectations. There is 
no specific treatment. A glycerin extract of the culture of 
the tubercle bacilli was first used by Koch, and it was found 
to exert a specific effect on tubercular inflammations. Injec¬ 
tions of one milligram were followed by intense constitu¬ 
tional and local reaction, and cures of external tuberculosis, 
such as lupus, were recorded. In internal tuberculosis, 
however, old quiescent lesions were stirred into activity, 
and acute miliary tuberculosis often developed from a local 
lesion. Various modifications of Koch’s lymph have been 
used, but they should be used with extreme caution. At 
present the feeling among the profession is strongly against 
the use of the lymph, but modifications and improvements 
may in the future place it among the standard list of specific 
drugs. 

Creosote, which has been gaining steadily in favor, is one 
of the best remedies in use. It may be given in 4-minim 
doses at first, gradually increased to 10 or 15 minims three 
times a day. It may be given with compound tincture of 
gentian or with glycerin and whiskey, and it should be 
diluted largely with water at the time of its administration, 
or it may be given in capsules. Only the pure beechwood 
creosote should be prescribed. The “ enteric pill ” of 
Parke, Davis & Co. contains creosote; it is not dissolved 
until it reaches the small intestine. The patient may wear 
continuously a perforated zinc inhaler (Robinson’s) kept 


TUBERCULAR DISEASES OE THE LUNG. 399 

moistened with equal parts of alcohol, chloroform, and 
creosote. Creosote may also be given by the rectum, from 
5 to 20 drops being mixed with the white of one egg and 
water and given every day. Guaiacol or the carbonate of 
creosote may be used in substitution. Iron, strychnine, 
and arsenic are useful tonics in combination, to combat the 
anaemia and to build up the general strength. The hypo- 
phosphites are useful tonics, but they have no specific 
action. 

Injections of antiseptics into the diseased pulmonary 
tissues have been advocated warmly; they are not com¬ 
monly employed, however, as bad results have occasionally 
followed their use. 

In some cases the inhalation of compressed air has been 
of great service. 

3. To Relieve Symptoms. —Fever, as a rule, is best treated 
by change of climate and by fresh air. When the tempera¬ 
ture is high, however, patients should not attempt much 
exercise, and frequently they do better when put to bed for 
a few days. Sponging with cool water relieves the fever¬ 
ishness and makes the patient comfortable, but other more 
radical measures are to be used with extreme caution. 

For the sweating, aromatic sulphuric acid is the best and 
the simplest remedy. Sponging the body with vinegar and 
water upon retiring is frequently effective. Zinc oxide, gr. 
ij, with ext. hyoscyami, gr. iij, in pill is a favorite combina¬ 
tion, while atropine in doses of gr. y^o- at night is fairly 
steady in its effects. Picrotoxin (gr. -g 1 ^-) may be used, but 
with extreme caution. Strychnine is often of use. Cough, 
if not too troublesome, is best left alone. If it be dry or 
harassing, opium or codeine may be given at night to secure 
sleep. Hydrocyanic acid, belladonna, and the expectorants, 
in combination with codeine, often relieve this troublesome 
symptom, but care should be taken that the stomach be not 



400 MANUAL OF THE PRACTICE OF MEDICINE. 


disturbed by nauseant remedies. If the cough be accom¬ 
panied with profuse expectoration, the expectorants are not 
indicated, but reliance should be placed upon creosote, tur¬ 
pentine and its derivatives, and the mineral acids. 

Pain in the chest is to be treated by counter-irritation. 

For the treatment of haemoptysis see Pulmonary Hem¬ 
orrhage. 

Diarrhoea should be treated on general principles, but 
opium in some form has almost always to be used. 


4. DISEASES OF THE PLEURA. 

FIBRINOUS OR DRY PLEURISY; PLASTIC 

PLEURISY. 

Etiology. —This form of pleurisy may be primary or sec¬ 
ondary. The primary form may appear to be due to expos¬ 
ure to wet and cold, but modern theories regard cold merely 
as a predisposing factor to bacterial infection. The second¬ 
ary form complicates any acute or chronic pulmonary disease 
involving the periphery of the lung. Thus, pleurisy occurs 
in conjunction with pneumonia with abscess, gangrene, or 
cancer of the lung, and with hemorrhagic infarctions. 
Occurring with pulmonary tuberculosis and phthisis, it may 
be the earliest indication of tubercular disease, and many 
cases of so-called “ primary pleurisy ” owe their origin to a 
small undiscovered tubercular lesion in the lung that may 
finally develop and give rise to symptoms. 

Pleurisy may be secondary to inflammation of organs 
other than the lungs. Thus, pleurisy may arise from caries 
of the ribs or of the vertebrae, from perforation of an oeso¬ 
phageal cancer, from tubercular disease of the bronchial 
glands, from pericarditis, or from peritonitis. Cases follow¬ 
ing erysipelas of the chest-wall are not infrequent. 



FIBRINOUS OR DRY PLEURISY. 


401 


Patients with gout and with Bright’s disease are more 
subject to pleurisy than are others. A pleurisy develops 
during the course of acute rheumatism, the pleura being 
involved, as are other fibro-serous membranes, as one of 
the regular manifestations of the disease. The belief is 
gaining ground that pleurisy, after all, results from the action 
of various micro-organisms, the most common of which are 
the streptococcus pyogenes, the pneumococcus, and the 
bacillus tuberculosis. Probably there are many other micro¬ 
organisms capable of causing the disease, and further bac¬ 
terial examinations are desirable to enable cases of pleurisy 
to be grouped according to their microbic cause. 

Pathology.—The pleura becomes congested, dry, and loses 
its normal lustre. Fibrin and serum infiltrate the thickness 
of the pleura and make their way to the free surface, so that 
the pleura is coated with a layer of lymph of variable thick¬ 
ness. The exudate may be shaggy in appearance or may 
be thick and stratified. Microscopically, the fibrinous exu¬ 
date consists of fibrin, leucocytes, red blood-cells, and 
serum. The serum, however, is but slight in amount and 
undergoes rapid absorption. Subsequently the exudate 
becomes absorbed or becomes organized into connective 
tissue, so that the pleura is thickened and adherent to the 
opposing pleural surface. 

Dry pleurisy usually begins in the pulmonary pleura and 
is limited to a small area. The opposing pleural surface 
usually is involved secondarily. 

Symptoms.—The symptoms of secondary pleurisy are 
often masked by those of the primary disease. Pain in 
the side and the friction rale are the only characteristic 
symptoms. 

In primary cases the attack may begin with a chill and 
with fever rarely over 102° F. The pain, which is sticking 
or stabbing in character, is referred to the site of the pleu- 
26 


402 MANUAL OF THE PRACTICE OF MEDICINE. 

risy. The pain is rendered worse by deep breathing or by 
coughing. There may be tenderness in the intercostal 
spaces over the lesion. The breathing is rapid and shallow, 
and there may be a dry, painful cough which is of reflex 
origin. In mild cases a stitch in the side on deep breathing 
may be the only symptom. 

Physical Signs.—The characteristic physical sign of dry 
pleurisy is the pleural friction sound, which may be crepi¬ 
tant or subcrepitant or which may resemble a moist mucous 
rale. The crepitant rale is a fine dry crackle or shower of 
crackles heard at the end of inspiration only; it arises only 
in the pleura. A subcrepitant rale is a fine, moist, sticky 
sound, heard with inspiration, with expiration, or with 
both. Mucoid rales may arise from the rubbing together 
of surfaces covered with very moist lymph; they may ex¬ 
actly simulate the bronchial rales. 

The differential diagnosis between pleural and bronchial 

rales is as follows: 


Pleuritic Rales. 

1. May be of the crepitant variety. 

2. Sound superficial, directly under 
the ear. 

3. Fairly constant. 

4. Not influenced by coughing. 

5. Over local area, which does not 
alter its position. 

6. All of one variety. 


Bronchial Rales. 

1. Never the crepitant variety. 

2. Sound “ deep in.” 

3. Very inconstant. 

4. Influenced by coughing. 

5. May be over large areas or in 
shifting areas. 

6. Usually assorted rales of all kinds. 


The occurrence and diagnosis of the pleuro-pericardial 
friction sound has been described under Pericarditis (p. 187). 

The absence of pleuritic rales does not necessarily ex¬ 
clude pleurisy, as the rales may come and go, may only 
appear on deep breathing, and may, moreover, arise at areas 
which are deeply seated, as in diaphragmatic or mediastinal 
pleurisy. 

The duration of the disease is from three to ten days. 




PLEURISY WITH EFFUSION. 


403 


The prognosis of the attack itself is good, but a broader 
view must be taken than that of mere temporary recovery. 
The cause and the significance of the pleurisy and the 
sequelae that may result from a thickened and adherent 
pleura must be considered. 

Treatment.—During the attack the patient should be 
kept quiet, but need not necessarily be confined to the bed, 
or even to the house, unless the symptoms be severe. 
Counter-irritation by cupping, by iodine, or by blisters often 
diminishes the pain and checks the spread of the inflamma¬ 
tion. Hot poultices are not so efficient as ice-bags applied 
locally. In all cases a brisk purgative should be given at 
the start, preferably calomel or magnesium sulphate. For 
the pain morphine may be given, and the chest may be 
strapped with adhesive plaster as for fractured rib, to dimin¬ 
ish the friction between the inflamed pleural surfaces. In 
rheumatic cases salicylic acid or its derivatives should be 
given in full doses, as for acute articular rheumatism. 

PLEURISY WITH EFFUSION. 

Etiology and Synonym.—The etiology of sero-fibrinous 
pleurisy is the same as that of the plastic form. The former 
seems, however, to be due to a severer form of bacterial infec¬ 
tion. Pulmonary tubercular disease follows, in time, one- 
third of the so-called “ primary ” cases. Synonym : Sero¬ 
fibrinous pleurisy. 

The pathology of the sero-fibrinous is the same as that 
of the plastic form, except that there is added an excessive 
exudation of serum ; moreover, the inflammation involves a 
larger area than in dry pleurisy. The exuded fluid is of a 
composition resembling that of blood-serum; its color is 
citron-yellow, and it may be clear, or somewhat turbid from 
flocculi of fibrin or from leucocytes and desquamated cells 
from the pleural surface. Blood may be present from rup- 


4 04 MANUAL OF THE PRACTICE OF MEDICINE . 

ture of fine blood-vessels or in the case of cachectic and 
debilitated subjects. The amount of the exudation varies 
greatly. An amount under 300 cubic centimeters does not 
give rise to physical signs in an adult. From one to two 
pints is the usual quantity, but eight to ten pints may be 
exuded. The exudation sinks to the dependent portions of 
the pleural sac unless encapsulated by previously existing 
adhesions—a somewhat rare occurrence in sero-fibrinous 
pleurisy. The fluid in the pleural sac rarely changes its 
level with any change in the position of the patient, being 
practically encapsulated by fibrinous adhesions between the 
lung above and the costal pleura. The upper level does 
not follow the ordinary laws of water-level, but follows a 
curve to which the name of “ Garland’s S-curve is given. 

Mechanical Effects of the Effusion. —The lung floats 
upward, its base resting on the fluid. As the fluid takes the 
place of the lung in the pleural vacuum, the lung is free to 
shrink, from its own elastic retraction, until the pleural sac is 
two-thirds full of fluid ; when this point is reached the lung 
is in a condition of elastic equilibrium. Any excess of 
fluid over this amount exerts a direct pressure on the lung, 
so that in extensive effusions the lung is compressed, form¬ 
ing a dense, airless, carnified mass at the dome of the pleu¬ 
ral cavity. The heart is bodily displaced to the opposite 
side, but it undergoes no twisting upon its axis, so that 
kinks in the great vessels do not occur. The diaphragm 
is sagged downward, and in right-sided pleurisy the liver 
is depressed. The intercostal spaces bulge, especially in 
children, and the affected side measures from one-half to 
one inch more than the other side. 

The symptoms are inflammatory and mechanical. 

1. Inflammatory symptoms may occur acutely or sub- 
acutely. If the onset be sudden, there may be a chill, 
which, however, is never so severe as in pneumonia. The 


PLEURISY WITH EFFUSION. 


405 


temperature rises to from ioi° to 103° F., attains its maxi¬ 
mum on about the third day, and slowly subsides, reaching 
the normal in from seven to ten days. The temperature is 
fairly continuous, not remittent as in empyema, and there is 
no definite crisis. Persistence of the fever after two weeks, 
or a temperature higher than 104° F. at any time, suggests 
empyema or tuberculosis. Prostration is in proportion to 
the severity of the inflammation and the fever. The pulse 
is rapid and compressible. Pain is marked at the onset, but 
it becomes less marked as the effusion is poured out, sep¬ 
arating the opposing inflamed pleural surfaces. There may 
be a reflex cough with a scanty mucous expectoration. If 
the onset be insidious, the inflammatory symptoms are less 
marked. The chill is absent, the fever is rarely over ioi° 
or 102 0 F., and prostration is so slight that the patient is 
up and frequently is able to work. 

2. Mechanical symptoms depend upon the amount of the 
effusion and upon the rapidity with which it is poured out. 

Dyspnoea results from the pleuritic pain and from the 
diminished expansion of the lung. It may be present only 
on exertion, or it may be so extreme as to be most distress¬ 
ing. The more rapidly the effusion is poured out, the more 
marked is the dyspnoea. 

The position of the patient in bed is often suggestive. 
Before the effusion is poured out he lies upon the sound 
side, so as not to press the inflamed pleural surfaces together 
by his weight. After the effusion occurs he lies upon the 
affected side, so that the weight of the fluid will not embar¬ 
rass the action of the heart or of the sound lung. 

Cyanosis is likely to occur in cases with large effusions, 
and the heart’s action may be weak and irregular. 

The physical signs may be described as occurring before 
effusion, during the effusion, and after absorption of the 
effusion. 


406 manual of the practice of medicine. 

Before the effusion the friction rales of dry pleurisy are 
present, expansion is limited, and the percussion-note may 
be slightly dull. 

During the Effusion.— There is an important distinction 
to be made between the physical signs of moderate and 

those of excessive exudation. 

i. The signs of moderate effusion begin to appear when 
the exudation reaches ten or twelve ounces in adults or 
three or four ounces in children. 

(a) Below the level of the fluid there should be diminished 
expansion, slight bulging of the intercostal spaces, espe¬ 
cially in children, and an in¬ 
creased girth of the affected 
side. The percussion-note 
is flat, the upper limit of flat¬ 
ness describing “ Garland’s 
S-curve.” This curve begins 
low in the back, rises to its 
highest point in the axilla, 
and then sinks with a slight 
descent to the sternum. The 
upper line of flatness is rarely 
influenced by a changed position of the patient. In left- 
sided pleurisy flatness replaces the normal tympany of 
Traube’s semilunar space. Below the line of the fluid 
the voice and the breathing are muffled and even lost, and 
vocal fremitus should be absent. It is claimed that the 
whispered voice may be transmitted through serous, but 
not through purulent, effusions (Baccelli’s sign). 

Exceptionally , below the level, voice and breathing may 
persist, though distant and indistinct; pleuritic rales may 
be heard through adhesions persisting below the level. 
In children soft bronchial voice and breathing may be 
heard, even if there be no compression of the lung. In 






PLEURISY WITH EFFUSION. 


40; 


some cases, especially in aged subjects, the percussion- 
note may be dull or dull-tympanitic below the fluid. Vocal 
fremitus may persist below the level, from adhesions extend¬ 
ing downward through the effusion, or the fremitus may be 
transmitted along the chest-wall from the lung above or 
from the opposite side. 

( b ) At the level of the fluid there should be dulness and 
pleuritic rales. Exceptionally, a bleating of the voice 
(oegophony) is heard, being elicited by having the patient 
pronounce the words “want” or “plant.” CEgophony, 
however, is a sign of rare occurrence. Pleural rales may 
be absent at the line of fluid. 

(c) Above the level of the flidd , in moderate effusions, the 
physical signs may be normal, or there may be a tympanitic 
percussion-note with feeble breathing. Tympany in these 
cases is due to relaxation of the lung-tissue; it is most 
marked under the clavicle, constituting “ Skoda’s sign.” In 
some cases in children the note under the clavicle may even 
be of the “ cracked-pot ” order, and may lead to the erro¬ 
neous diagnosis of a cavity, especially as cavernous breathing 
may be heard, by reason of a large bronchus approaching 
the chest-wall owing to the retraction of the lung. Both 
bronchial and pleural rales are often heard over the retracted 
lung. 

(d) Signs of Displaced Viscera. —In left-sided pleurisy the 
apex beat of the heart may be under the sternum, so that 
it cannot be appreciated, or in more abundant effusion it 
may be displaced as far as the right nipple. In right-sided 
pleurisy the apex beat may be as far to the left as the mid¬ 
axilla. Over the apex of such a displaced heart a systolic 
murmur may be heard. In right-sided pleurisy the lower 
border of the liver is felt by palpation below the free border 
of the ribs in the mammary line. 

2. The signs of excessive exudation differ from the preced- 


408 manual of the practice of medicine . 

ing physical signs in that the lung begins to be actually 
compressed. Over the compressed lung the note is dull- 
tympanitic or dull, the breathing and the voice become 
broncho-vesicular or bronchial, and vocal fremitus is in¬ 
creased. There may be loud bronchial rales of a guigling 
quality. As the lung begins to be compressed “ Garland s 
S-curve ” becomes less marked until finally the uppei limit 
of the flatness is a straight horizontal line. Below the level 
of the fluid the percussion-note is flat, and breathing and 
voice are of a soft, distant, bronchial character, being trans¬ 
mitted down the tense chest-wall from the compiessed lung 
above. In the same manner vocal fremitus may be trans¬ 
mitted down the chest-wall over the fluid, although, as a 
rule, vocal fremitus is absent in these cases. The chest is 
usually motionless on inspiration, the intercostal spaces are 
bulged or tense, mensuration shows an increased growth of 
from one to one and a half inches, and the displacement of 
the heart and the liver becomes evident. 

Patients with the above physical signs are often treated 
for pneumonia, but a mistake in diagnosis should not occur, 
for, if doubt exist, the aspirating-needle should be used. 

As the effusion becomes absorbed the physical signs of fluid 
disappear and breathing is heard to the base of the chest. 
The friction rale usually reappears. Some dulness on per¬ 
cussion and feeble breathing with friction rales persist for 
months, from thickening of the pleura. 

In every case of doubt an aspirating-needle should be in¬ 
serted, with the strictest antiseptic precautions, below the 
supposed level of the fluid. Fluid may not appear at the 
first introduction of the needle, should its calibre be blocked 
by a bit of fibrin. The use of the aspirating-needle not only 
makes positive the diagnosis of fluid, but it determines the 
character of the fluid—whether serous, hemorrhagic, or 
purulent. 


PLEURISY WITH EFFUSION. 


4O9 


Course of Pleurisy with Effusion.— 1. The onset may 
be acute, both inflammatory and mechanical symptoms being 
pronounced. Inflammatory symptoms subside in from 
seven to ten days ; later the effusion becomes absorbed or 
is removed, mechanical symptoms disappear, and the patient 
recovers. 

2. In other cases the inflammatory symptoms subside, 
but the fluid remains unabsorbed and mechanical symptoms 
persist. 

3. Other cases begin as pleurisy with effusion, but grad¬ 
ually septic symptoms develop. The fever becomes high 
and remittent; there are erratic chills and night-sweats with 
rapid emaciation. The aspirating-needle shows the fluid to 
have become purulent from an added infection by pus cocci. 
These cases, however, are rare. 

4. The onset may be insidious. Inflammatory symptoms 
are not marked, but mechanical symptoms gradually in¬ 
crease. These patients are the ones who feel “ run down ” 
and short of breath on exertion, and who come to the hos¬ 
pital with a chest half full of fluid. 

5. There may be a double pleurisy. These cases are 
usually of tubercular origin. Their course is persistent and 
insidious, and pericarditis is a frequent complication. 

Sudden death is a rare termination, being more common 
with the severer cases of pleurisy. Post-mortem examina¬ 
tion shows in some cases congestion and oedema of the 
lungs, and in others an ante-mortem heart-clot, while in 
other cases no pathological cause can be found. 

Sequelae.—In some cases the pleura returns to a prac¬ 
tically normal condition. In others the pleura is left thick¬ 
ened and adherent and may lead to the following com¬ 
plaints : 

1. Local tenderness, worse on exertion or in damp 
weather. 


410 MANUAL OF THE PRACTICE OF MEDICINE. 


2. Reflex cough. 

3. Pain and slight dyspnoea on exertion. 

4. There may be developed in the course of time— (a) 
chronic bronchitis; (b) emphysema; (c) interstitial pneu¬ 
monia; (a) chronic pleurisy, with the formation of new 
connective tissue; or (e) recurring attacks of pleurisy with 
fibrin or with effusion. 

The heart may remain fixed in its abnormal position by 
adhesions, or it may ultimately be displaced to the affected 
side by retraction of pleuritic adhesions. 

The prognosis for the attack itself is good. Neglected 
cases in which the lung has been compressed may, how¬ 
ever, do badly. The ultimate prognosis should consider 
the underlying cause of the pleurisy and the possibility of 
sequelae arising from pleural thickening and from adhesions. 

Treatment.—During the inflammatory stage the patient 
should be put to bed and be kept on a light diet. Pain 
should be treated by counter-irritation, strapping, hot or 
cold applications to the chest, and, if necessary, by opium 
by the mouth or subcutaneously. Painful cough is to be 
relieved by sedatives. In rheumatic cases salicylates, with 
or without potassium iodide, may be given. 

The treatment of the mechanical symptoms is designed 
to get rid of the effusion, and a choice of two methods pre¬ 
sents itself: 

The reduction of the effusion may be accomplished by 
free purgation and diuresis. The best cathartic for the pur¬ 
pose is magnesium sulphate in doses of from 1 to 1^ 
ounces, given every second morning, an hour before break¬ 
fast, in a concentrated form. The choice of the proper 
diuretic is simply empirical: one after another should be 
tried, singly or in combination, until the desired effect is 
accomplished. The diet should be concentrated, and only 
a minimum quantity of water should be allowed. 




PURULENT PLEURISY. 


411 

Withdrawal of the effusion by aspiration is the most sat¬ 
isfactory treatment, and it should be resorted to under the 
following conditions: (1) A sudden large effusion with 
dyspnoea and cyanosis. (2) A large effusion with marked 
mechanical symptoms. (3) Should the physical signs of 
compression of the lung be found. Aspiration in these 
cases should be done without delay. (4) Should the effu¬ 
sion be uninfluenced by catharsis and diuretics. Absorp¬ 
tion proceeds better, even if but little fluid be withdrawn. 
It certainly seems wrong to waste much time and debili¬ 
tate the patient with exhausting treatment when so safe and 
efficient a means of relief may be used. 

To aspirate, the patient should be semi-recumbent. 
Stimulants should be at hand, and the strictest asepsis 
should be employed. The needle is inserted below the 
level of the fluid, usually in the eighth space in the axillary 
line, and the fluid is withdrawn slowly. No more than 50 
ounces should be withdrawn at any one time, and the opera¬ 
tion should be stopped at once if severe pain, dyspnoea, 
faintness, or paroxysmal cough develop. The danger of 
aspiration is sudden heart failure, but this is exceedingly rare. 
After aspiration the remaining fluid is usually absorbed, but 
occasionally the fluid reaccumulates, and it must be removed 
by a second or even a third aspiration. 

PURULENT PLEURISY (EMPYEMA). 

Etiology. —Purulent pleurisy is regularly due to the 
infection of the pleural cavity by some micro-organism 
capable of exciting suppuration. Infection is due to the 
following bacteria in order of frequency: Streptococci, 
pneumococcus, tubercle bacilli, staphylococci, Eberth’s 
bacilli, and the saprophytic bacteria of gangrene. These 
micro-organisms may infect in pure cultures or in combi¬ 
nations (mixed infection). 


412 MANUAL OF THE PRACTICE OF MEDICINE . 

Infection is permitted by—(i) Penetrating wounds of the 
chest-wall, or by the use of a septic aspirating-needle; 
(2) gangrene, abscess, or septic emboli of the lung, ruptured 
tubercular cavities, or perforation of the oesophagus; (3) in¬ 
fection through the diaphragm following abscess of the 
liver or peritonitis; (4) secondary to pneumonia and to 
some acute infectious diseases, as scarlet fever, typhoid, 
measles, whooping-cough, and “ grippe.” 

Pathology.—The lesion of purulent pleurisy is the same 
as that of pleurisy with serous effusion, except that pus- 
cells infiltrate the thickness of the pleura and are found in 
the effusion in varying amounts. The exudate may be 
sero-pus, or thick and creamy, or of a greenish or yellowish 
color. The odor is usually mawkish, but it may be foul or 
gangrenous. A peculiar yeasty odor is noticed in many 
cases of pneumococcus infection. The effusion is more apt 
to be sacculated than that of serous exudation, and compres¬ 
sion of the lung is more apt to occur. Subsequent changes 
may occur in the pleura, in the effusion, and in other viscera. 

Changes in the Pleura .— 1. In rare cases, especially in 
children and in pneumococcus infection, with prompt 
removal of the exudate the pleura may return to a healthy 
condition. 

2. The pleura may become thickened and adherent after 
the removal of the fluid. 

3. The pleura may be thickened; its surface is composed 
of granulation-tissue secreting pus, constituting a pyogenic 
membrane. 

4. In the pleura may be deposited the salts of lime. 

5. The pleura may become necrotic in places and slough. 
By the extension of the necrotic processes the pus may find 
its way through the chest-wall (empyema necessitatis), or 
through the diaphragm, or it may rupture into the lung or 
the pericardium, 


PURULENT PLEURISY. 


413 


Changes in the effusion result by an added infection of 
putrefactive germs, usually those of gangrene of the lung. 
The effusion becomes foul and offensive, and gases of 
decomposition may form, constituting pyo-pneumothorax. 
Small purulent effusions may become inspissated and infil¬ 
trated with lime-salts. 

Changes in other viscera are those changes common to pro¬ 
longed suppuration. There may be amyloid degeneration 
of the spleen, the liver, and the kidneys, or chronic diffuse 
nephritis. 

Symptoms of inflammatory and mechanical origin are 
present, resembling those of fibrino-serous pleurisy, but in 
empyema septic symptoms are added, consisting of erratic 
chills, high remittent temperature, cold sweats, prostration, 
diarrhoea, emaciation, and the development of a septicaemic 
or typhoid condition. 

1. The onset may be sudden, with inflammatory and 
mechanical symptoms. There are a chill, fever, pain in the 
side, prostration, dyspnoea, and the physical signs of pleural 
effusion. The case resembles at first fibrino-serous pleurisy, 
but the aspirating-needle draws pus. Later, septic symp¬ 
toms develop. 

2. The onset may be insidious. Inflammatory symptoms, 
such as initial chill and fever, are not marked, but mechani¬ 
cal and septic symptoms slowly develop. The patient is 
indisposed and has pain in the side, slight fever, and dysp¬ 
noea. The fever becomes higher and is remittent. Erratic 
chills, cold sweating, and prostration become marked. 

3. If empyema follow pneumonia, there is usually an 
attempt at crisis. The temperature, however, rises again 
and becomes remittent, dyspnoea develops, septic symptoms 
appear, and the physical signs of a pleural effusion make 
their appearance. Chills, however, are not common in pure 
pneumococcus infection of the pleura. 


414 MANUAL OF THE PRACTICE OF MEDICINE. 


Course of the Disease.— I. Some patients die during the 
acute onset, from the intensity of the inflammation. 

2. Septicaemia may be developed in early cases, especially 
if the effusion undergoes putrefactive changes. 

3. Some patients pass into a hectic condition and die in 
several months, exhausted or in the typhoid condition. 

4. Death may result from the primary diseases, as phthisis, 
gangrene, or abscess of the lung. 

5. Death may result from perforation into the pericar¬ 
dium or the peritoneum. If rupture into a bronchus occurs, 
pus will be expectorated, with a relief of all the symptoms. 
Owing to poor drainage, the improvement is usually tem¬ 
porary. In rare cases, however, spontaneous cure has been 
effected. 

Aspiration of the pus into the bronchi at the time of rup¬ 
ture may cause asphyxia or septic broncho-pneumonia, and 
pneumothorax may develop by air entering the pleural cav¬ 
ity through the bronchial fistula. 

If rupture through the chest-wall occurs, the opening is 
usually in the fifth or sixth interspace in front. Drainage 
is usually poor, and improvement is but temporary. Spon¬ 
taneous cure may, however, result, with or without the for¬ 
mation of a thoracic fistula. 

6. Small circumscribed empyemata may terminate by 
gradual absorption, by thickening and calcification of the 
pleura, and by local chest-retraction. 

The physical signs are in the main those of fibrino-serous 
pleurisy. Mention, however, should be made of a few addi¬ 
tional points: 

The interspaces are apt to be obliterated more than in 
simple pleurisy, and they may even bulge. There may be 
oedema of the chest-wall. Whispered speech is not usually 
transmitted through purulent effusions. 

In children distinct bronchial breathing may be heard 


PUR ULENT PLE UR IS V 41 5 

over a large purulent effusion, so that a mistaken diagnosis 
of pneumonia frequently is made. 

Pulsations of the effusion synchronous with the cardiac 
systole (pulsating empyema) is sometimes observed, for which 
no satisfactory explanation can be offered. Of 42 cases, 39 
occurred on the left side. 

Prognosis.—Empyema is a very serious affection, the 
severity of which largely depends upon the particular 
micro-organism to which it is due. Infection by the pneu¬ 
mococcus is regularly less severe than that caused by the 
streptococci. Cases due to the saprophytic bacteria of 
gangrene afford the worst prognosis. The prognosis is 
better in children than in adults, in cases promptly treated 
than in those allowed to progress, and in cases with slight 
sepsis. The prognosis also depends upon the general con¬ 
dition of the patient and the nature of the primary disease. 



The treatment of empyema is that of an abscess requir¬ 
ing incision and drainage. Cases due to simple infection by 
pneumonia, especially in infants, may recover after aspiration, 
but, as a general rule to which there are but few exceptions, 
aspiration should not be resorted to except as a temporary 







































































41 6 MANUAL OF THE PRACTICE OF MEDICINE. 

measure. Incision and drainage should be insisted upon, 
no matter how desperate the patient’s condition may seem. 
The details of the operation are to be found in text-books 
on surgery. Irrigation is permissible only with putrid or 
gangrenous empyema. Chest-gymnastics calculated to in¬ 
duce deep inspiratory efforts are of value in convalescence. 
The method of Ralston James, of forced expiratory efforts, 
is to be advised to expand the retracted lung. By the 
arrangement of the water-bottles shown in Figure 42, water 
may be forced from one bottle into the other by blowing 
into the mouth-piece. This process should be repeated a 
number of times daily. 

Should the lung not expand, and should a thoracic fistula 
result from the operation, Estlander’s operation may be per¬ 
formed. This operation consists in the resection of one or 
more inches of several ribs in the lateral aspect of the chest. 

CHRONIC PLEURISY. 

Etiology and Synonyms.—A thickened and adherent 
condition of the pleura may result from acute pleurisy, 
causing, in some cases, diminished chest-expansion, pain 
aggravated by deep breathing or by cold and damp weather, 
and possibly a reflex cough. Aside from these symptoms, 
cases are met with in which the pleura is the seat of a pro¬ 
gressive and chronic inflammation, to which the name 
“ chronic pleurisy” should more properly be applied. Chronic 
pleurisy may follow acute pleurisy, whether plastic, fibrino- 
serous, or purulent, or the inflammation may be chronic 
from the start. Synonyms: Chronic adhesive pleurisy; 
Pleurisy with the production of new connective tissue. 

Pathology.—Two forms of the disease are described : 

1. Chronic Dry Pleurisy .—The lesion is usually confined 
to one pleura, but it may be bilateral. The pleura is thick¬ 
ened by growth of connective tissue, so that it may exceed 


CHRONIC PLEURISY. 


417 


one-half or even three-fourths of an inch in thickness, and the 
opposing pleural surfaces are adherent. This form of pleu¬ 
risy occurs most extensively after empyema, is one of the 
regular lesions of chronic pulmonary phthisis, and in rare 
cases may appear at the base as a primary disease. 

2. Chronic Pleurisy zvith Effusion. —The pleura is thick¬ 
ened ; there is a serous effusion which in many cases is sac¬ 
culated, the encapsulated serum being encysted by thick¬ 
ened and adherent pleura. In cases following empyema 
there may be collections of inspissated pus containing lime- 
salts. The lung, which may be invested with thickened pleura 
preventing its full expansion, maybe the seat of a bronchitis 
or of a chronic interstitial pneumonia with or without bron¬ 
chiectasis. The heart may be displaced to either side. 

The symptoms at first are slight. There is a pleuritic 
pain, worse on deep breathing and in damp weather, fre- 
qently associated with tenderness in the overlying intercostal 
spaces. Dyspnoea on exertion results from diminished 
chest-expansion \ it is more marked in cases with serous 
effusion. There may be a cough of reflex origin or due to 
a complicating bronchitis. The patient loses flesh and 
strength and becomes anaemic. These symptoms become 
more and more marked as the disease progresses. 

Physical Signs.—Inspection shows retraction of the 
chest-wall and diminished expansion. If the pleurisy be 
dry, there will be dulness or flatness according to the thick¬ 
ness of the pleura and the strength of the percussion-blow. 
Breathing and voice-sounds are muffled, distant, or absent 
altogether. Vocal fremitus is diminished or lost, but pleu¬ 
ritic fremitus may be marked on forced inspiration. Auscul¬ 
tation reveals pleuritic rales, creakings, and old rubbing 
friction sounds. 

If there be fluid, the physical signs of pleural effusion will 

be present, although the signs are often obscured by those 
27 


41 8 MANUAL OF THE PRACTICE OF MEDICINE. 

of the surrounding thickened pleura, especially if the effu¬ 
sion be encapsulated. There may be added the physical 
signs of bronchitis, bronchiectatic cavities, and interstitial 
pneumonia. 

The diagnosis of thickened pleura from fluid is to be 
made with certainty only by the use of the aspirating-needle. 
If the pleura be thickened, the needle is felt to pass through 
a firm, almost cartilaginous substance which gives a charac¬ 
teristic feeling of resistance. The diagnosis of chronic pleu¬ 
risy from new growths of the pleura often presents great 
difficulties. 

The course of the disease is slow and steady, extending 
over years. The patient is finally reduced to invalidism, but 
death almost always results from some intercurrent disease. 

Treatment consists (I) in building up the general health 
by good food, proper climate, and tonic medication; (2) in 
counter-irritation by iodine or by blisters; (3) by exercises 
destined to increase chest-expansion ; and (4) by the removal 
of serous accumulations in small quantities at a time. 

TUBERCULAR PLEURISY. 

Etiology.—The association of pleurisy, both plastic and 
with effusion, and pulmonary tuberculosis has elsewhere 
been described. Besides these cases the pleura may be the 
seat of a tubercular disease, either as one of the lesions of 
acute general miliary tuberculosis or as a localized lesion 
which may be primary or secondary to other tubercular 
deposits, especially in the bronchial glands. 

Pathology.—The lesions are usually confined to one side, 
but in rare instances they may be bilateral. 

1. The pleura is thickened with tubercular nodules, 
cheesy masses, and leucocytes, and miliary tubercles appear 
upon the free surface. The appearance of the pleura and 
the character of the effusion vary in different cases. 


TUBERCULAR PLEURISY. 


419 


0 ) The pleura may be deeply congested and be studded 
with miliary tubercles. 1 here is a hemorrhagic serous 
exudation. 

( P ) The pleura is studded with tubercles and covered by 
fibrin. There is a fibrino-serous effusion. 

( c ) The pleura is thickened with caseous and softening 
tubercular nodules, its surface is coated with fibrin, pus, and 
cheesy matter, and it may present tubercular ulcerations. 
The effusion is purulent and contains little cheesy masses 
and shreds of the pleural tissue. It is remarkable that in a 
large proportion of these cases neither tubercle bacilli nor 
the germs of suppuration are found in the effusion ; but in¬ 
oculation of this apparently sterile fluid in animals is fre¬ 
quently followed by the development of tubercles. 

2. There may be a tubercular dry pleurisy thus described 
by Osier: “ Both parietal and costal layers are greatly 
thickened—perhaps from two to three millimeters each— 
and present firm fibroid caseous masses and small tubercles, 
while uniting these two greatly thickened layers is a red¬ 
dish-gray fibroid tissue, sometimes infiltrated with serum. 
This may be a local process confined to one pleura, or it 
may be in both.” These cases are frequently combined 
with a similar condition of the pericardium and the peri¬ 
toneum. 

The symptoms of tubercular pleurisy resemble in char¬ 
acter those of the non-tubercular forms, but run a slow, 
insidious course. Acute cases are rare. 

Diagnosis is made by attention to the following particu¬ 
lars: (1) There is usually some antecedent tubercular his¬ 
tory, or evidences of a pre-existing tubercular disease. 
(2) The onset of the pleurisy is insidious. (3) The course 
of the disease is progressively bad. (4) The fluid does not 
disappear with medication: it persistently reaccumulates 
after aspiration. (5) Emaciation and prostration are out of 


420 MANUAL OF THE PRACTICE OF MEDICINE. 

proportion to the local disease. (6) Aspiration shows a 
purulent effusion containing cheesy matter in which tuber¬ 
cle bacilli may be found, or the serum may be hemorrhagic. 
If cancer of the pleura and laceration of the lung by the 
point of the needle be excluded, the occurrence of a hemor¬ 
rhagic serum is almost diagnostic of tubercular pleurisy. 

Duration. —Rare acute cases may terminate in two weeks. 
The usual duration is from three to six months or even longer. 

The prognosis is regularly fatal. 

Treatment consists in building up the general health by 
the rules laid down for the treatment of tuberculosis, and in 
the withdrawal of the fluid by aspiration when it accumu¬ 
lates. Should the effusion become purulent, the case should 
be treated as one of empyema—by incision and drainage. 

PNEUMOTHORAX; HYDRO-PNEUMOTHORAX; 

PYO-PNEUMOTHORAX. 

Etiology. —Pneumothorax arises—(i) From perforation 
of the chest-wall following penetrating wounds, incision for 
the drainage of empyema, or empyema necessitatis. (2) 
From the perforation of the pulmonary pleura by rupture 
of the lung by violence, by overstraining, or by injury from 
careless aspiration; or there may be rupture of emphy¬ 
sematous vesicles. Air may dissect down the peritracheal 
connective tissue, from violent coughing attacks following 
tracheotomy whenever the tube becomes blocked, and may 
rupture into the pleural cavity. One fatal case of the writer’s 
occurred in this way. Rupture of a tubercular cavity is the 
direct cause of 90 percent, of all cases of pneumothorax. Less 
common are the cases due to septic broncho-pneumonia, 
abscess or gangrene of the lung, hemorrhagic and septic 
infarcts, and rupture of an empyema into a bronchus. (3) 
From the perforation of other organs, as from cancer of the 
oesophagus, the stomach, or the colon. The accident may 


PNE UMO THORAX. 


421 


follow perforation through the diaphragm of a subphrenic 
pyo-pneumothorax. 

Pathology.—When air enters, the pleural vacuum is at 
once destroyed, and the lung shrinks by reason of its own 
elasticity, the heart is displaced bodily toward the opposite 
side, and the liver sags downward, exceeding the down¬ 
ward displacement observed in pleural effusion. If the point 
of perforation remain open, the intra-pleural air is at atmo¬ 
spheric pressure, and the lung is not compressed. If the 
orifice of rupture be valve-like (ventilating pneumothorax), 
air can enter during inspiration, but its exit during expira¬ 
tion is prevented, so that the intra-pleural pressure becomes 
raised and the lung becomes compressed and carnified. 
The point of rupture may be large, constituting a pleuro- 
bronchial fistula, especially in long-continued cases, or it 
may be small, baffling detection on post-mortem examina¬ 
tion. If the orifice of rupture be closed by a contraction 
of the lung or by a deposit of fibrin, the intra-pleural air may 
be at any degree of tension. The question of tension is of 
importance in the understanding of the physical signs. 

In rare cases the entering air is sterile, and a simple pneu¬ 
mothorax results; usually, however, infection and inflam¬ 
mation of the pleura result in the formation of a serous 
effusion (hydro-pneumothorax) or of pus (pyo-pneumo¬ 
thorax), the latter condition being far the more common. 
The effusion sinks to the dependent portion of the pleural 
cavity; its upper level is a straight horizontal line (there 
being no Garland’s S-curve, as with pleurisy with effusion), 
and the level of the fluid changes regularly with the vary- 
ing position of the patient. In rare instances the orifice of 
perforation is surrounded by pleural adhesions, so that a 
localized sacculated pyo-pneumothorax results. 

Symptoms.—The symptoms may be sudden and urgent 
or may be latent or obscure. 


422 MANUAL OF THE PRACTICE OF MEDICINE. 


1. If pneumothorax occur in a fairly healthy patient, the 
onset is sudden and alarming. There is a severe pain in 
the side, with a feeling that “ something has given way." 
There is extreme dyspnoea, amounting to agonizing air- 
hunger, with cyanosis in some cases, and aphonia “ for want 
of breath ” is usually observed. Symptoms of surgical 
shock rapidly develop—lividity, prostration, cold, clammy 
skin, feeble and rapid heart-action—and death may result 
from shock within a few hours. Should the patient survive, 
the symptoms of shock slowly disappear. Dyspnoea con¬ 
tinues, with rapid, insufficient breathing. The patient sits 
up with the body inclined to the affected side. There are 
evidences of poor circulation—lividity, dropsy, or venous 
congestions. Pain in the side continues, and the symptoms 
of pleural effusion make their appearance. Death finally 
results from exhaustion, from sepsis, or from pre-existing 
disease. 

2. If pneumothorax occur in a person much debilitated 
by phthisis or by pulmonary gangrene, the symptoms are 
obscured. Increased dyspnoea and enfeebled heart-action 
may be the only additional symptoms. In some cases sud¬ 
den death results. In rare cases, in healthy adults with 
pneumothorax, the disease runs this insidious and obscure 
course. 

3. If the pneumothorax be due to rupture of pulmonary 
air-vessels after severe straining efforts, the air is usually 
absorbed, but inflammation of the pleura with serous effu¬ 
sion almost regularly results. 

Physical Signs.—On inspection the affected side is en¬ 
larged and motionless. Vocal fremitus is diminished or lost. 
The percussion-note depends upon the tension of the intra¬ 
pleural air. If the air be at low tension, the note will be 
tympanitic or amphoric. If there be a free pleuro-bronchial 
fistula, a “ cracked-pot ” note may be obtained. If the intra- 


PNE UMO THORAX. 


423 


pleural air be at high tension, the percussion-note will be 
dull-tympantic, dull, or even flat. Percussion over a pneu¬ 
mothorax frequently gives the sensation of percussing an 
air-cushion. Flatness is obtained over the effusion; the 
upper limit of the flatness is horizontal and changes accord¬ 
ing to the position of the patient. 

Breathing- and voice-sounds may be feeble and distant, 
contrasting with the exaggerated breathing-sounds over the 
sound side ; or there may be a distant inspiratory murmur 
of amphoric quality. When the orifice of rupture admits 
air freely, voice and breathing may be typically amphoric. 

Should the lung be compressed, there will be bronchial 
voice and breathing over the carnified lung, heard with less 
distinctness over the air. The Hippocratic succussion con¬ 
sists of loud splashing sounds heard when the patient is 
violently shaken. Similar sounds may occur, however, 
when gas and fluid are shaken in a distended stomach. 
The metallic tinkle consists of clear tinkling sounds resem¬ 
bling those produced by striking a pin against a thin glass 
tumbler. The “ penny-click ” of Trousseau is one of the 
most characteristic physical signs of pneumothorax. A coin 
pressed firmly in an intercostal space in front is tapped with 
another coin while the auscultator listens at the back of the 
chest: the transmission of a metallic echoing sound is 
characteristic of a large air-cavity ; it is not, however, path¬ 
ognomonic of pneumothorax. 

Aid is afforded in diagnosis by the physical signs of dis¬ 
placed liver and heart. 

The diagnosis is usually easy. Mistakes may arise by 
confusing pneumothorax with— {a) Large phthisical cavities 
at the base of the lung. Here the penny-click is not heard, 
succussion is rarely obtained, pleuritic rales are heard gen¬ 
erally over the area, and the heart and the liver are not dis¬ 
placed. There are, moreover, no sudden urgent symptoms. 


424 MANUAL OF THE PRACTICE OF MEDICINE. 


( b ) Diaphragmatic hernia following crush or injury. ( c ) Sub- 
phrenic pyo-pneumothorax. 

Prognosis. —But few cases of pneumothorax recover. 
The prognosis depends upon the cause, the septic character 
of the infection of the pleura, the general condition of the 
patient, the presence of pre-existing disease, and the severity 
of the shock and the reaction. 

Duration.—The ordinary duration of the disease is be¬ 
tween two and three months. Patients may die in shock 
in a few hours, while in rare cases the disease becomes 
chronic and extends over months or years. 

Treatment. —At the time of the perforation morphine or 
chloroform may be given for the pain, and the symptoms 
of shock may be treated on general principles. Where 
effusion forms, the case should be dealt with as ordinary 
pleurisy with effusion or as empyema—by aspiration, or 
incision and drainage. In pyo-pneumothorax occurring in 
advanced phthisis it may be the better course simply to 
remove the pus by aspiration rather than to render the last 
days of the patient uncomfortable by a surgical operation. 

NEW GROWTHS OP THE PLEURA. 

The majority of new growths in the pleura are of second¬ 
ary nature and complicate tumors of the lung or the chest- 
wall, the pleura being directly invaded by the new growth. 
Of the primary new growths of the pleura, endothelial 
carcinoma is the most important. The pleura is infiltrated 
and studded with scattered nodules, or the cancer may be 
diffuse. Pleurisy is developed with fibrino-serous effusion, 
which in 12 per cent, of all cases is of a hemorrhagic char¬ 
acter. Secondary metastatic growths may occur in the 
lungs, in the bronchial glands, or in distant organs. 

The symptoms resemble those of chronic pleurisy with 
effusion. Pain, however, is more continuous and severe, 


HYDROTHORAX. 


425 


and there may be exquisite tenderness in the intercostal 
spaces. The effusion may be hemorrhagic, and cancerous 
cachexia develops. 

Diagnosis. —Aid in diagnosis may be afforded by the 
presence of malignant tumors elsewhere. The diagnosis 
in the earlier stages may with difficulty be made from 
chronic tubercular pleurisy. 

The physical signs are those of thickened pleura with 
effusion. 

The prognosis is invariably fatal. 

The treatment is simply symptomatic. If sarcoma of 
the pleura be suspected, hypodermic injection of the toxic 
products of erysipelas germs may be employed. 

HYDROTHORAX. 

Etiology. —Hydrothorax occurs with dropsy of other 
organs, with nephritis, with diseases of the heart, and with 
profound anaemia; it may result from pressure of a tumor 
upon an intrathoracic vein. 

Pathology. —The lesion of hydrothorax consists of an 
accumulation of serum in the pleural cavity, without inflam¬ 
mation of the pleura itself. In the cases due to nephritis 
or to anaemia the lesion is usually bilateral. In heart dis¬ 
ease one cavity alone is involved in the majority of instances ; 
if both cavities are implicated, however, the amount of the 
fluid in the two sides is not equal. Intrathoracic pressure 
on a vein regularly results in unilateral hydrothorax. The 
fluid is simple serum without inflammatory ingredients, the 
pleural surfaces are normal, and the amount of effusion is 
rarely excessive. 

The symptoms are often obscured by those of the pri¬ 
mary disease. Dyspnoea is, however, increased by the trans¬ 
udation, and it may be associated with cyanosis and great 
distress. Pain and fever are absent. 


426 MANUAL OF THE PRACTICE OF MEDICINE. 


The physical signs are those of pleural effusion. The 
friction rale is not heard, however, and, as fibrinous adhe¬ 
sions do not exist, the fluid is more apt to change its level 
with the varying position of the patient than is common in 
fibrino-serous pleurisy. Compression of the lung rarely, 
if ever, occurs. 

The prognosis is that of the primary disease. 

The treatment also is that of the primary disease. The 
dropsies are to be treated by heart-stimulants, diuretics, and 
cathartics. If the breathing be embarrassed by the trans¬ 
udation, and no relief follows medicinal measures, repeated 
aspirations are to be resorted to. 

HEMOTHORAX. 

Etiology.—Hemorrhage into the pleural cavity may 
occur from rupture of an aneurysm, from erosion of an 
intrathoracic vessel, or from injuries resulting in fractures 
of the rib or in laceration of the lune. 

Pathology.—The blood may coagulate and be absorbed 
if not too excessive in amount. If infection occurs, there 
may be pleurisy with effusion or empyema. 

The symptoms are those of hemorrhage—pallor, dysp¬ 
noea, thready pulse, sighing respirations, and restlessness, 
associated with pleuritic pain and dyspnoea. Symptoms of 
pleurisy with effusion or of empyema may develop in in¬ 
fected cases. 

The physical signs are those of pleural effusion. The 
friction rale is, however, absent. 

Prognosis.—A large haemothorax, such as arises from 
rupture of an aneurysm, is rapidly fatal. Small hemorrhages, 
especially those due to injury, may terminate in absorption 
and recovery. 

The treatment is that of acute anaemia—by transfusion, 
warmth to the extremities, and small doses of opium. A 


L YMPH ADENITIS. 


427 


small hmmothorax is best left alone. If the clot be infected 
or be large enough to interfere with respiration, it may be 
evacuated by incision. 


5. DISEASES OF THE MEDIASTINUM. 

LYMPHADENITIS. 

Simple lymphadenitis follows inflammations of the lungs 
or the bronchi, especially in children. More rarely the con¬ 
dition arises in the course of some infectious diseases, espe¬ 
cially typhoid fever and diphtheria. 

The lesion consists of swelling and congestion of the 
gland, resulting either in resolution or in enlargement. 
Suppuration rarely occurs. Not infrequently the glands 
become secondarily infected by the tubercle bacilli. 

The adhesion of an enlarged gland to the oesophagus 
may result in a traction-diverticulum. 

The symptoms are rarely observed. In some cases bron¬ 
chitis with paroxysmal cough results from congestion and 
irritation of the neighboring structures. 

Suppurative lymphadenitis may follow simple or tuber¬ 
cular inflammation of the glands. The pus may finally be 
inspissated, infiltrated with lime-salts, and encapsulated, or 
it may rupture into the bronchi or the oesophagus. 

Tubercular lymphadenitis regularly accompanies tuber¬ 
cular lesions in the lung. In other cases the glands filter¬ 
ing out the impurities gaining entrance to the lungs may 
primarily be infected. The tubercular glands may attain a 
large size and may cause the pressure-symptoms of a medi¬ 
astinal tumor. The caseous masses may become inspis¬ 
sated and encapsulated, or they may rupture into neighbor¬ 
ing organs. The lungs, the pleura, or the pericardium may 



428 MANUAL OF THE PRACTICE OF MEDICINE. 


be involved secondarily by extension. General tuberculous 
infection so commonly results, especially in children, that 
search should be made for tubercular glands of the medias¬ 
tinum in every case of acute miliary tuberculosis of obscure 
origin. 


MEDIASTINAL TUMORS. 

Of 520 cases of mediastinal tumor reported by Hare, 
cancer occurred in 134, sarcoma in 98, and lymphoma in 
21. Less frequently are found dermoid and hydatid cysts, 
fibroma, lipoma, gumma, and enchondroma. Growths 
formed by the aggregation of tubercular glands and aneur¬ 
ysms have previously been described. Cancer may be 
primary or secondary. Sarcoma is more apt than cancer 
to be primary, men are more frequently affected than women, 
and the majority of cases occur between the twenty-fifth and 
fortieth years. 

The symptoms are due to increasing intrathoracic pres¬ 
sure. Dyspnoea is the most marked symptom ; it is due to 
pressure on the trachea, the recurrent laryngeal nerve, the 
lungs, or the bronchi. In the latter stages of the disease 
orthopncea is usually developed. Cough may be parox¬ 
ysmal, resembling that of whooping-cough, or there may be 
a brassy co.ugh as with aneurysm. Pressure on the thoracic 
duct occasions rapid emaciation. Dysphagia occurs if the 
oesophagus be compressed. Compression of the thoracic 
veins results in cyanosis of the chest, the arms, the head, 
and the neck, and in extraordinary attempts to establish 
collateral circulation. Congestion and oedema of the lung 
may be occasioned by pressure on the pulmonary vein. 
Pleural effusion is apt to appear either by an involvement 
of the pleura by the new growth or from pressure of the 
tumor on the vena azygos or on one of the intercostal veins. 

Pain is not as common with tumor as with aneurysm. 


MEDIASTINAL TUMORS. 


429 


Physical Signs.— There is evident dyspnoea. Some 
valuable aid in localizing mediastinal new growths is 
afforded by noticing what position of the patient best re¬ 
lieves the pressure-symptoms and modifies the dyspnoea. 
There may be blueness of the upper part of the body and 
arms, while the enlarged thoracic and anastomosing abdom¬ 
inal veins stand forth prominent and distended. According 
to Osier, the distention and enlargement of the thoracic veins 
are more marked with lymphadenoma than with cancer or 
with sarcoma. The sternum or the intercostal spaces on 
either side may be bulged forward or may be involved by 
the growth. A transmitted expansion frequently suggests 
aneurysm, but it is not so marked, there is no lateral expan¬ 
sion, and there is no diastolic shock. The tracheal tug is 
seldom if ever obtained, and over the tumor no murmur is 
detected, as in the latter disease. Dulness is elicited by 
percussion over the growth, either over the upper sternum 
or between the spinal column and the scapula in case of 
involvement of the posterior mediastinum. The breathing 
on either side may be feeble from bronchial compression or 
may assume a tubular character. The physical signs are 
modified by the signs of pleural effusion or of cancer of the 
lung or the pericardium. 

Diagnosis. —Many points of differential diagnosis from 
aneurysm of the aorta have already been alluded to. In 
many cases a positive diagnosis cannot be given, although, 
should the patient live over eighteen months, a malignant 
mediastinal growth may probably be excluded. 

The prognosis depends upon the nature of the growth. 

Treatment. —In cases of lymphoma the administration 
of arsenic is often followed by a diminution of the growth. 
For radical cure surgical treatment alone can avail, but as 
this is rarely possible, the medicinal treatment is merely 
palliative, to quiet the pain and to relieve the dyspnoea. 


430 MANUAL OF THE PRACTICE OF MEDICINE. 

Opium may be given without conscientious dread of form¬ 
ing a habit. 

ABSCESS OF THE MEDIASTINUM. 

This affection is usually of traumatic origin ; it may, how¬ 
ever, be secondary to infectious fevers, to pyaemia, to ery¬ 
sipelas, or to suppurative disease of the adjacent viscera. 
Chronic abscesses are usually of tubercular origin. The 
abscess, which is usually situated in the anterior medias¬ 
tinum, is more common in males than in females. The pus 
may finally become inspissated and encapsulated, or it may 
rupture through the sternum, through an intercostal space, 
or into the oesophagus or the trachea, or it may burrow into 
the abdominal cavity. 

The symptoms are those of abscess and pressure. Pain 
is marked from the start, is of a throbbing character, and is 
associated with exquisite tenderness. Irregular fever, chills, 
and sweating mark the presence of pus. Cough, dysphagia, 
and dyspnoea occur as pressure-symptoms. 

The prognosis must be guarded, owing to the possible 
complications. 

Treatment.—In the earlier stages the ice-bag or the cold 
Leiter coil should be employed continuously. When pus 
has formed it may be evacuated by trephining the sternum. 

EMPHYSEMA OF THE MEDIASTINUM. 

This condition is met with in trauma, follows the oper¬ 
ation of tracheotomy, and may result from rupture of the 
peripheral air-vesicles of the lung during violent cough¬ 
ing or straining. Air may enter the cellular tissue of the 
mediastinum by perforation of ulcers of the trachea, the 
bronchi, or the oesophagus. The. emphysema may be 
limited to the mediastinum, may rupture into the pleura, 


DISEASES OF THE THYMUS GLAND. 


431 


causing pneumothorax, or may spread to the neck and even 
to the entire body. The treatment is entirely symptomatic. 

MEDIASTINAL HEMATOMA. 

Hemorrhage into the mediastinal tissues occurs in hemor¬ 
rhagic conditions, from erosion or rupture of blood-vessels 
or from rupture of an aneurysm. 

The symptoms are those of hemorrhage and mediastinal 
pressure, while ecchymoses may appear after a few days in 
the lumbar region. 

DISEASES OF THE THYMUS GLAND. 

Hypertrophy is occasionally met with in children; it 
may cause spasm of the glottis (thymic asthma) or sudden 
death. 

Abscess may develop in syphilitic children. 

Sarcoma and carcinoma may originate in the thymus 
gland and may give the regular symptoms of tumor in the 
mediastinum. The gland may be enlarged during the course 
of leukaemia or of Hodgkin’s disease. 

Hemorrhages in the gland-tissue are not uncommon dur¬ 
ing scurvy and purpura haemorrhagica. 


IV. DISEASES OF THE DIGESTIVE 

SYSTEM. 


i. DISEASES OF THE CESOPHAGUS. 

ACUTE (ESOPHAGITIS. 

Etiology. —The oesophagus may be inflamed— (i) by 
the spread of inflammation from the pharynx or the 
stomach; (2) by mechanical or chemical irritants or corro¬ 
sives; (3) by pseudo-membranous inflammation secondary 
to diphtheria or to some acute infections ; (4) by the pus¬ 
tules of variola; (5) in rare cases oesophagitis may develop 
in sucklings without known cause. 

Lesions. —The inflammation may be diffuse or localized, 
and either catarrhal, pseudo-membranous, or phlegmonous. 
The pustules of variola result in ulcerations. There may 
be a mycotic inflammation secondary to thrush and resem¬ 
bling it in its pathological features. The swallowing of cor¬ 
rosives is followed by sloughing and ulceration. 

Symptoms. —Pain on swallowing is a nearly constant 
symptom, and a continuous substernal ache is frequently 
observed. Food may be regurgitated; if coated with blood 
or with pus, ulceration is indicated. 

In cases of caustic poisoning the lips, the mouth, and the 
pharynx exhibit evidences of corrosion, and the symptoms 
of toxic gastritis are present, usually with some associated 
shock. Rupture of the oesophagus may occur. Patients 
recovering from the acute symptoms ultimately develop 
oesophageal stenosis. 

432 



STENOSIS OF THE (ESOPHAGUS. 


433 


Some cases of acute oesophagitis, even if severe, occa¬ 
sion but a trifling amount of discomfort. 

The treatment of acute oesophagitis consists in the 
administration of the proper antidote in case of corrosive 
mineral poisons. Demulcent drinks and cracked ice are 
of service in diminishing the pain and the inflammation. 
The nourishment should be bland and unirritating. Fluids 
alone should be given during the acute stages, while in 
severe cases rectal alimentation should be insisted upon. 

CHRONIC (ESOPHAGITIS. 

A chronic catarrhal inflammation of the mucous mem¬ 
brane lining the oesophagus is produced by improper and 
irritating food and by the presence of tumors or stricture 
of the oesophagus itself; or the chronic form may result 
from an acute attack. 

The symptoms consist chiefly in the raising of mucus- 
coated regurgitated or vomited food. 

The treatment is that of the underlying cause. 

STENOSIS OF THE (ESOPHAGUS. 

Synonym.—Stricture of the oesophagus. 

Stenosis may result—(i) From compression from without by 
tumor of the neck or the mediastinum, by aneurysm, by re¬ 
tropharyngeal abscess, or by a large pressure-diverticulum. 
(2) From obstruction of the lumen by foreign bodies, and rarely 
by tumors and polypi. (3) From contraction of the wall, (a) 
There may be cicatricial contraction following the healing 
of ulcers due either to corrosive poisons or to diphtheria, 
small-pox, or, more rarely, to syphilis or to tubercular dis¬ 
ease. A rare form of ulceration, the “ round ulcer,” is seen 
at the lower end of the oesophagus. This ulcer is produced 
by self-digestion by regurgitated gastric juice, after the man¬ 
ner in which ulcer of the stomach is caused, (b) There 
28 




434 MANUAL OF THE PRACTICE OF MEDICINE . 

may be malignant growth of the wall, usually epithelioma. 
(c) There may be spasmodic contraction or (d) congenital 
narrowing at some part. 

Symptoms. —In all cases of stenosis of the oesophagus 
these cardinal symptoms are present—difficulty in swallow¬ 
ing, pain, and the regurgitation of food. The cases may, 
however, conveniently be described in three groups. 

Cicatricial Stenosis. 

The stricture may occur at any part of the oesophagus, 
but it is most frequent in the lower third. The whole 
length may be involved. The stenosis may reach such a 
degree that liquids can barely trickle through. The 
oesophagus above the stricture is usually much dilated, 
and its walls are thickened. 

After the history of antecedent ulceration the patient 
complains of increasing difficulty in swallowing, the food 
being - cut finer and finer and washed down with water. In 
severe cases liquids alone are taken. The food seems to 
stick, and after a time it is regurgitated. The lower down 
the stricture is, and the more dilated the oesophagus above 
it, the longer the time after eating before regurgitation 
occurs. The ejected food may be macerated and mixed 
with mucus, but that it has not reached the stomach is 
proved by the absence of gastric odor and by the alkaline 
reaction of the food. The latter test, however, is not infal¬ 
lible if the food be retained some hours before being regur¬ 
gitated, because of the formation of fatty acids in it. Pain 
is not a marked feature except at the time of swallowing 
the first bolus. 

The diagnosis is made by the passage of the oesophageal 
bougie. A conical bougie on an elastic whalebone stem 
should be employed, but the soft-rubber stomach-tube may 
be used. It is of the utmost importance, before passing the 


STENOSIS OF THE (ESOPHAGUS. 


435 


bougie, to exclude aortic aneurysm producing stenosis by 
compression, because of the danger of causing rupture of 
the aneurysmal sac. The tube should never be passed 
when ulceration of the oesophagus from any cause is sus¬ 
pected. Auscultation is frequently serviceable in cases 
where the bougie cannot be employed. The auscultator, 
listening to the left of the dorsal spine while the patient 
swallows a mouthful of water, hears a loud splashing, gurg¬ 
ling sound at the site of the stricture, below which the 
sound is absent or only slightly audible after a pause. 

The prognosis depends upon the degree of stenosis and 
upon its dilatability. In advanced grades death may ensue 
from inanition or from rupture of the dilated oesophagus 
above the stricture; or, should the regurgitated food enter 
the larynx, suffocation or aspiration-pneumonia may result. 

Treatment.—Gradual dilatation by the persistent use of 
the oesophageal bougie should be employed, and in many 
cases the results are remarkably good. The diet should 
be compact and nourishing, and rectal alimentation may 
be resorted to. In advanced cases the stricture may be 
cut, or an opening may be made into the oesophagus 
below the stricture (cesophagostomy), or into the stomach 
(gastrostomy). 


Cancerous Stricture. 

This form of oesophageal stricture is usually primary. 
Epithelioma is most common; scirrhus and encephaloid 
are rare. The growth usually occurs in the lower third, 
next in frequency in the upper third, of the oesophagus. Be¬ 
ginning in the mucous membrane, it extends to form an 
annular constriction, usually involving one or two inches 
of the tube. Ulceration of the growth may occur, so that 
the stenosis becomes less marked, but the ulceration may 
extend and perforate the lung, the trachea, a bronchus, the 


436 MANUAL OF THE PRACTICE OF MEDICINE. 

mediastinum, the aorta, or the pericardium. Erosion of 
the vertebrae may occur. Secondary growths in adjacent 
lymphatic glands are common. The oesophagus above the 
cancer is usually dilated, and its walls are thickened. 
Epithelioma is seen in patients over forty years of age; 
it is more common in men than in women. 

The symptoms resemble those of the cicatricial gioup in 
their essential features. Dysphagia is progressive, and it 
becomes so extreme that emaciation and inanition rapidly 
result. The regurgitated food frequently contains blood 
and pus in small quantities, and it may contain cancer-cells 
and fragments. Pain is a marked feature, being aggravated 
by attempts at swallowing. The cervical lymph-glands are 
enlarged, and symptoms of cancerous cachexia are present. 
The oesophageal bougie must be used with extieme caution 
to avoid penetrating the ulcerated wall, as such an accident 
has not infrequently occurred. The soft-rubber tube is 
generally preferable in these cases. 

The diagnosis is made positive by the finding of cancer- 
fragments in the eye of the tube. In cases of ulceration of 
the epithelioma in which no real degree of stenosis longer 
persists, the tube may pass without difficulty. In these 
cases, however, dysphagia and regurgitation of food may 
be nearly as marked as if there were an actual narrowing of 
the lumen; these symptoms are to be explained on the 
theory that downward peristalsis is checked at the site of 
the growth, and that a reversed peristalsis results in regur¬ 
gitation. 

The prognosis is hopeless. Patients usually die, from 
inanition, perforation, or aspiration-pneumonia, about one 
year after the symptoms begin to be noticed. 

The treatment consists in the proper feeding of the 
patient by nourishing liquid and concentrated food, by feed¬ 
ing through a stomach-tube or by the rectum. Gastrotomy 


STENOSIS OF THE CESOPHAGUS. 437 

or cesophagotomy offers but little chance even of prolong¬ 
ing life. 


Spasmodic Stenosis (CEsophagismus). 

This form of oesophageal stenosis occurs chiefly in young 
hysterical women or in those with marked neurotic tenden¬ 
cies. It may occur after an attack of choking, or as a 
nervous affection in those bitten by dogs and in dread of 
hydrophobia. It may occur from reflex causes, such as 
pregnancy, and it often complicates organic lesions of the 
oesophagus itself. 

The lesion consists of spasm of the oesophageal wall, 
usually at either the pharyngeal or the cardiac extremity. 
In the former case it is often associated with spasm of the 
pharyngeal muscles. 

The symptoms consist of inability to swallow, regurgi¬ 
tation of food, and a sense of substernal pain or constriction. 
The dysphagia comes on abruptly and is not progressive— 
two characteristics which distinguish the spasmodic from 
the other forms of stenosis. There are, moreover, periods 
of marked improvement; or the dysphagia may be only for 
certain articles of food, varying in individual cases. The 
inability to swallow is never so extreme as to endanger the 
life of the patient by inanition, although the disease may 
last for days, weeks, or even for months. Intermissions, 
however, usually mark the protracted cases. Associated 
hysterical or hypochondriacal symptoms are usually pres¬ 
ent, rendering the diagnosis the more evident. 

The prognosis is perfectly good. 

The treatment consists in passing the oesophageal bougie. 
Difficulty may be encountered by reason of the spasm, but 
patience and gentleness will usually succeed in accomplish¬ 
ing its passage. Often a brilliant cure follows the first treat¬ 
ment, but in obstinate cases a daily passage of the bougie 


438 MANUAL OF THE PRACTICE OF MEDICINE. 

may be needed, usually before the principal meal, to restore 

the confidence of the patient. 

Sedatives, such as valerian, the bromides, and phenacetine, 
may be given, and tonic treatment is indicated in nearly 

every case. 

DILATATIONS AND DIVERTICULA. 

Dilatation may be primary or secondary. 

Primary dilatation , which is rare, is due to a congenital 
defect in the muscular tissue of the oesophageal wall or to 
its paralysis. The oesophagus is enormously dilated and is 
usually longer than normal. The principal symptom is 
dysphagia from lack of sufficient peristalsis. 

Secondary dilatation occurs with stenosis above the point 
of constriction. The condition is to be suspected if apatieni 
with organic stricture of the oesophagus regurgitate laige 
quantities of macerated food. The retention of such quan¬ 
tities of food may cause pressure-symptoms. 

Diverticula are of two forms : 

Pressure-diverticulum. —This form is most common at the 
posterior wall of the oesophagus, at its junction with the 
pharynx. From weakness of the muscle at this point a 
bulo-ine of the mucous and submucous coats takes place, 
forming a hernial sac, into which food passes. Owing to lack 
of expulsive power, food collects and becomes macerated, the 
sac growing larger and larger. The sac may be emptied from 
time to time by contraction of the muscles of the neck or 
by external manipulation. It may be large enough, when 
full, to press forward and occlude the oesophagus. 

The diagnosis is made by the presence in the neck of a 
tumor which can be emptied by manipulation, and by alter¬ 
nately passing the bougie down the oesophagus and into 
the sac. 

Traction-diverticulum. —This form is situated on the ante- 


VARIX OF THE (ESOPHAGUS . 


439 


rior wall of the oesophagus, opposite the bifurcation of the 
trachea. Should the mediastinal glands normally present 
at this point become inflamed, they will enlarge and may 
become adherent to the wall of the oesophagus ; by the 
subsequent contraction of the glands the wall is drawn 
out into a funnel shape, never more than a quarter of an 
inch in depth. This form gives no symptoms, although in 
rare cases perforation has been known to occur. 

PARALYSIS OP “THE (ESOPHAGUS. 

This rare condition develops from diseases of the brain 
and the cord, from hysteria, and occasionally as a post- 
diphtheritic paralysis. 

The symptoms consist of difficulty in swallowing. The 
passage of the bougie reveals, however, no stricture. 
Paralytic dilatation may subsequently be developed. 

The treatment consists in nourishing the patient by the 
stomach-tube, in treating the original cause, and in faradi¬ 
zation of the oesophagus. 

RUPTURE OP THE (ESOPHAGUS. 

This accident may occur during violent and sudden at¬ 
tempts at vomiting in healthy people, but it is exceedingly 
rare, rupture usually being due to the perforation of an 
oesophageal ulcer or of a foreign body. 

The condition is fatal within a few days, and treatment is 
merely symptomatic. 

VARIX OP THE (ESOPHAGUS. 

Varicose veins may develop in the lower portion of the 
oesophagus, as an evidence of congestion, of heart disease, 
or of cirrhosis of the liver. Chronic oesophagitis with vomit¬ 
ing of mucus usually results, and rupture of the varicose 
veins may lead to fatal hemorrhage. 


440 MANUAL OF THE PRACTICE OF MEDICINE. 


2. DISEASES OF THE STOMACH. 

ACUTE CATARRHAL GASTRITIS. 

Etiology and Synonyms.—Among the causes predis¬ 
posing to acute catarrhal gastritis may be enumerated 
lesions of the heart or of the liver causing chronic conges¬ 
tion of the stomach, and any condition of depreciated health 
or of fever that renders it difficult for the stomach to digest 
the food properly. Gouty individuals are apt to suffer from 
gastritis, and personal idiosyncrasy often plays an important 
role. The exciting cause is usually a dietetic error—over¬ 
feeding ; eating when too tired to digest properly; food 
unsuitable for digestion, as hot bread, unripe fruit, or.food 
improperly cooked. Over-indulgence in alcohol is a frequent 
cause. Severe attacks follow the taking of irritants or of 
tainted meat or fish, poisoned ice-cream, poor milk, or unripe 
fruit. Certain articles of diet, varying with each individual, 
may precipitate an attack. Gastritis is frequently symp¬ 
tomatic of an infectious disease or fever. Synonyms: 
Acute gastric catarrh; Acute indigestion. 

Pathology.—The mucous membrane of the stomach is 
swollen, congested, and covered with tenacious mucus. There 
may be small submucous hemorrhages or small superficial 
erosions. The cells of the gastric tubules are swollen and 
cloudy, and the interglandular tissue may be infiltrated with 
leucocytes. Hydrochloric acid is usually temporarily absent 
from the gastric secretion, being replaced by lactic acid and 
the fatty acids. The most frequent seat of inflammation is 
near the pylorus, and the inflammation may extend to the 
duodenum or, especially in children, may involve the entire 
small intestine. 

The symptoms are divided clinically into two sets of 
cases: 


ACUTE CATARRHAL GASTRITIS. 


44I 


1. Simple Gastritis (Acute Indigestion ).—The appetite is 
lost or is diminished except for highly-seasoned food. 
There are uncomfortable feelings referred to the stomach, 
in some cases amounting to severe colicky pain. Nausea 
is frequently complained of, and vomiting usually affords 
relief. The vomited matters, which consist of undigested 
food mixed with mucus and bile, are of an acid reaction 
from the presence of lactic and fatty acids. The patient 
complains of headache, depression, and prostration. The 
tongue is coated and the breath is offensive. The bowels 
are usually constipated, although diarrhoea may follow the 
attack. Fever usually is slight, although in some cases 
the temperature may reach 102° or 104° F. The abdomen 
is usually somewhat distended and tender in the epigastric 
region. Herpes, urticaria, or erythema may appear, espe¬ 
cially in cases caused by eating shell-fish. 

In young infants vomiting, fever, and prostration are the 
principal symptoms. In the symptomatic gastritis of infec¬ 
tious disease, vomiting and increased prostration are the 
prominent symptoms. The vomiting may be so excessive 
as to interfere with the nourishment of the patient. 

2. Gastritis from Ptomaine-poisoning .—This form of gas¬ 
tritis follows the eating of tainted meat or fish or of ice¬ 
cream containing the alkaloidal poison tyrotoxicon. Cases 
frequently occur in small epidemics among those who have 
eaten of some particular article of food. 1 he symptoms are 
those of a severe gastritis, with marked prostration and in¬ 
cessant vomiting. In severe cases constitutional symptoms 
of an alarming nature appear; the pulse becomes rapid, the 
heart’s action feeble, the skin becomes cold and clammy, 

and the patient is apt to die. 

Treatment of Gastritis. — The first indication is to lid the 
stomach of whatever is irritating it. Nature often does this 
by the vomiting, otherwise a simple emetic is usually indi- 


442 MANUAL OF THE PRACTICE OF MEDICINE. 

cated. The bowels should be opened, castor oil or saline 
laxatives usually being employed for this purpose, although 
blue mass or calomel is often beneficial. A natural diarrhoea 
should not be checked. Should it be excessive and exhaust¬ 
ing, a dose of castor oil (sss) and tincture of opium (HI xv) 
in combination should be given. The diet should be light 
and easily digestible. These rules suffice for the majority 
of mild cases. In more severe cases the stomach should 
have a rest and food should be interdicted for a day, 
although cracked ice and carbonated waters may be given 
freely. When the vomiting is constant, rectal alimentation 
may be resorted to. Distressing symptoms should be con¬ 
trolled by appropriate medication. The vomiting should 
not be checked until the stomach is empty; after that 
bismuth in full doses, bicarbonate of soda, oxalate of cerium, 
or even small doses of codeia or of morphine, may be given. 
Pain is best relieved by emesis, by counter-irritation over 
the stomach, by poultices or mustard pastes, and by the ad¬ 
ministration of large doses of bismuth. Codeia or hypo¬ 
dermic injections of morphine are to be given only in severe 
cases. Stimulants may be indicated in the gastritis of 
ptomaine-poisoning. 

TOXIC GASTRITIS. 

This form of gastritis follows the swallowing of concen¬ 
trated acids, alkalies, or irritants, frequently taken with 
suicidal intent, or of certain non-corrosive poisons like phos¬ 
phorus, arsenic, and antimony. In the former case the 
mucous membrane of the mouth, the oesophagus, and the 
stomach is marked with areas of necrosis surrounded by 
zones of intense inflammation, while the submucosa is 
hemorrhagic and infiltrated with serum. In severe cases 
perforation of the stomach may occur. In the non-corrosive 
poisons the process consists in fatty degeneration of the 


ACUTE CROUPOUS GASTRITIS. 


443 


glandular elements, small-celled infiltration of the entire 
glandular connective tissue, and hemorrhage. 

The symptoms are intense burning pain in the mouth, 
throat, and stomach, difficulty in swallowing, and constant 
vomiting, the vomited matters usually containing blood, and 
frequently containing portions of necrosed mucous mem¬ 
brane. The abdomen is distended and exquisitely tender. 
In very severe cases symptoms of collapse appear; the pulse 
is rapid and feeble, the skin is cold and clammy, and there 
is great prostration, frequently interrupted by restlessness 
or by convulsive movements. Albumin is usually present 
in the urine, and there may be hematuria. Perforation of 
the stomach is followed by death in collapse within a few 
hours. If the patient recovers there may result stricture 
of the oesophagus or extensive cicatrices in the stomach, lead¬ 
ing to chronic atrophy and inanition. 

The treatment is that of severe gastritis. Emetics should, 
however, not be given, on account of the danger of causing 
perforation. Siphonage of the stomach is preferable, a soft- 
rubber stomach-tube being passed with caution, and the 
stomach being washed with solutions of the appropriate 
chemical antidote. Hypodermic injections of morphine 
are needed to allay the pain and distress. Rectal alimen¬ 
tation is usually necessary; it should be resorted to in the 
severer cases. 

ACUTE CROUPOUS GASTRITIS. 

Synonyms.—Diphtheritic gastritis; Membranous gastritis. 

Croupous gastritis may occur as a secondary infection 
with diphtheria, but is more common as a secondary pro¬ 
cess in pneumonia, typhus and typhoid fever, pyaemia, puer¬ 
peral fever, and Asiatic cholera. 

The symptoms are those of an intense gastritis together 

with those of the primary disease. 





444 MANUAL OF THE PRACTICE OF MEDICINE . 

The diagnosis cannot be made during life. 

The treatment is that of the severer forms of gastritis. 

ACUTE SUPPURATIVE GASTRITIS. 

Etiology and Synonyms.—This uncommon disease oc¬ 
curs more often in men than in women. It is rare as a primary 
disease, usually occurring after pyaemia, puerperal fever, or 
other septic diseases. Synonyms: Phlegmonous gastritis; 
Purulent gastritis. 

Pathology.—The lesion, which consists in a suppurative 
process in the submucosa, presents itself in two forms—a 
diffused purulent infiltration, and a localized abscess; in the 
latter case rupture may occur into the stomach or into the 
peritoneal cavity. 

The symptoms are those of gastritis and of a severe in¬ 
fection. There is severe pain in the stomach, usually with 
exquisite tenderness in the epigastrium. If the abscess be 
large, it may be felt externally. Vomiting is persistent and 
agonizing, and the vomited matters may contain pus. Jaun¬ 
dice has occurred in a few instances. 

The symptoms of general infection are an irregular fever 
ranging between 102° and 105° F., rapid and feeble pulse, 
prostration, delirium, and finally coma. The disease may 
in rare instances run a subacute course, with pain, vomiting, 
irregular fever, and erratic chills. 

The diagnosis is made with the utmost difficulty, espe¬ 
cially in primary cases. Aid may be afforded if the abscess 
be large enough to be appreciated by the touch and if vom¬ 
iting of a large amount of pus occur. 

The treatment is simply palliative. 

MYCOTIC AND PARASITIC GASTRITIS. 

The invasion of the stomach by the bacillus of diphtheria 
and the pus organisms of phlegmonous gastritis has already 


CHRONIC CATARRHAL GASTRITIS. 


445 


been described. A fatal case of the growth of favus has 
been reported. The tubercle bacillus may involve the gas¬ 
tric mucous membrane, while sarcinae and the yeast fungus 
are frequently found in cases of fermentation and in dilated 
stomachs, and serve to increase the inflammation. 

Ascarides, taeniae, earth-worms, maggots, and the larvae 
of certain dipterae have been found to be the cause of acute 
gastritis. 


CHRONIC CATARRHAL GASTRITIS. 

Synonyms. —Chronic dyspepsia; Chronic gastric catarrh ; 
Atrophy of the stomach. 

Etiology. —The causes of chronic gastritis are various 
and may be classified as follows : 

Dietetic Causes .—Among these may be enumerated over¬ 
eating, over-indulgence in ice-water during meals, rapid 
eating, irregular meals, improperly cooked and unsuitable 
food, such as rich fried food, pastries, or hot bread, and the 
abuse of alcohol, tea, or tobacco. 

Constitutional Causes .—Chronic gastritis may be produced 
by any debilitating disease which reduces nervous force or 
deteriorates the blood. The food, not being digested prop¬ 
erly, is retained in the stomach, ferments, and sets up a 
chronic inflammation. In this way the gastritis is often 
associated with anaemia, chlorosis, tuberculosis, Bright's 
disease, diabetes, gout, and uterine disease. 

Local Causes .—The disease may be secondary to lesions 
of the stomach, such as cancer, ulcer, or dilatation, or it 
may follow passive congestion of the mucous membrane as 
in cirrhosis, or in any obstruction to the portal circulation, 
chronic heart disease, and certain diseases of the lung pro¬ 
ducing general venous congestions. 

Pathology. —Two forms of chronic gastritis are described, 
a simple and a sclerotic. 


446 MANUAL OF THE PRACTICE OF MEDICINE. 

Simple Chronic Gastritis. —The mucous membrane is 
thickened, is grayish or congested in appearance, and is 
covered with thick tenacious mucus. The veins are usually 
congested, and patches of pigmentation from small sub¬ 
mucous hemorrhages are common, especially near the 
pylorus. The membrane frequently has a granular or 
reticular appearance from irregular growth of connective 
tissue. The connective tissue and the muscular coats are 
usually also thickened, especially around the pylorus, and 
this thickening may be marked enough to cause a narrow¬ 
ing of that orifice. The gastric tubules are atrophied and 
deformed, their cells are cloudy and swollen, and between 
the tubules is an abundant small-celled infiltration. 1 here 
may be cystic dilatation of individual tubules. 

Sclerotic gastritis occurs as a final result of these paren¬ 
chymatous and interstitial changes and presents two dis¬ 
tinct forms : 

In the first form the stomach is usually dilated and its 
walls are thinned. The mucous membrane is thin, smooth, 
and light grayish in color; its glandular elements undergo 
fatty degeneration and atrophy. In advanced cases nothing 
remains of the mucous membrane but a layer of round cells, 
a few cysts, and fibrous tissue. This process is also called 
“phthisis ventriculi ” or “ simple atrophy.” 

The second form, “ cirrhotic atrophy,” which is even 
more rare than the first form, shows the same glandular 
destruction, but the walls are much thickened by enormous 
overgrowth of muscular fibres and connective tissue, and 
the whole organ diminishes greatly in size. In rare cases 
the thickening may be so great as to be felt through the 
abdominal walls. 

Symptoms.—Two clinical forms may be recognized, sim¬ 
ple gastritis and sclerotic gastritis , of which the former is by 
far the more common. 


CHRONIC CATARRHAL GASTRITIS. 


447 


Simple Gastritis .—Distress or oppression in the stomach 
is a fairly constant symptom; it may be slight, or less fre¬ 
quently it amounts to actual pain. It usually occurs after 
eating, but it may be more or less constant, and in some 
cases it is aggravated when the stomach is empty. In some 
cases the pain consists of a burning feeling under the ster¬ 
num, due to over-acidity, usually from the presence of the 
fatty acids of fermenting food; this pain is generally asso¬ 
ciated with eructations of a sour, acid fluid. To this con¬ 
dition the names “pyrosis,” “heartburn,” and “ cardialgia ” 
have been given (although the term “ pyrosis” has also been 
used as synonymous with “ water-brash ”). There may be 
tenderness over the stomach, more commonly diffused, and 
rarely severe. The appetite is usually impaired, although 
some patients complain of unnatural hunger. There may 
be appetite only for highly-seasoned and peculiar articles of 
food. Thirst is usually much increased. Flatulence is 
marked in the great majority of cases, producing distention 
of the abdomen, palpitation of the heart with intermittency 
of its action, a feeling of distress amounting at times to dysp¬ 
noea, and a stitching pain under the free border of the 
ribs. Relief is afforded by the eructations of gas, which 
may be odorless or offensive. There may be eructation of 
food or of fluid with the gas. The regurgitated food may 
be bitter or so acid as to set the teeth on edge; it may be 
associated with heartburn, or the fluid maybe clear, watery, 
brackish, and of an alkaline reaction. This latter form, 
which is termed “ water-brash ” (or “ pyrosis ” of some 
authors), is most commonly observed in the gastritis of 
drunkards. It usually occurs in the morning, being due to 
an increased amount of saliva which has been swallowed 
during the night. Nausea and vomiting are not usually 
pronounced. Nausea, when present, usually occurs in the 
morning, and it is especially common in alcoholic cases 


448 MANUAL OF THE PRACTICE OF MEDICINE. 

associated with “ dry retching. "V omiting usually occurs 
one or two hours after eating. The vomited matters consist 
of food in various stages of digestion and fermentation, 
mixed with mucus. Chemical examination shows diminu¬ 
tion or absence of hydrochloric acid, and abnormal acids, 
such as butyric, lactic, and acetic acids, are present. Small 
quantities of blood, either bright red, or in brownish gran¬ 
ules from alteration of its pigment, may be vomited from 
time to time. Digestion is usually much delayed, por¬ 
tions of food being present in the stomach as late as seven 
hours after eating, at which time a normal stomach should 
be empty. Absorption is slow, as is proved by the fact 
that iodide of potassium given in capsule is not found in the 
saliva in fifteen minutes, as is normally the case, but that it 
may not be in evidence for more than half an hour. The 
tongue is usually heavily coated and is indented by the 
teeth. The edges and the tip may be red, and in some 
cases the whole tongue has a “ raw-beef” appearance. The 
breath is usually offensive, and a bad taste in the mouth is 
complained of, especially in the morning. Saliva and the 
pharyngeal secretions are usually increased, and the patient 
may complain of a cough, the “ stomach-cough,” probably 
due to pharyngeal irritation. The bowels are usually 
constipated, but attacks of diarrhoea with the passage of 
undigested food may occur. The urine may be diminished 
in quantity, of high specific gravity, and may deposit uric 
acid, urates, phosphates, or oxalate of lime. The patient 
loses flesh and strength in accordance with the gravity of 
the case; this symptom is the most reliable means of esti¬ 
mating the true extent of the inflammation. From the 
passage of undigested fermenting food into the small in¬ 
testine, functional disturbance of the liver is induced, 
adding its symptoms. Among these symptoms may be 
cited hot and cold flashes, marked enough to suggest 


CHRONIC CATARRHAL GASTRITIS. 


449 


malaria to the patient, headache, dizziness, and inaptitude 
for mental and physical work. 

Sclerotic Gastritis .—There is an entire absence of digestive 
power of the stomach. Hydrochloric acid, pepsin, and 
milk-curdling ferment are all absent, and the fasting stomach 
is usually empty. I he symptoms are those of a severe 
dyspepsia with failure in nutrition. Vomiting is a prom¬ 
inent feature, and, associated with decided loss of flesh and 
ol strength, might suggest the existence of cancer. In other 
cases a progressive anaemia is developed, the symptoms re¬ 
sembling those of pernicious anaemia. In cases of “ cirrhotic 
atrophy” there may be inability of the stomach to hold 
more than a small amount of nourishment at any one 
time. 

Prognosis.—The course is essentially chronic, with 
periods of marked improvement from time to time. The 
symptoms often come and go, depending on the general 
health and upon the thoroughness and efficacy of the treat¬ 
ment. A guarded prognosis for recovery should always 
be given, especially if the disease has lasted any length of 
time. Relapses may be induced by trifling indiscretions. 
The danger of atrophy must be considered in severe and 
long-continued cases, for this condition tends to shorten 
life by inanition and anaemia. 

The treatment is (i) dietetic and hygienic, and (2) 
medicinal. 

1. Dietetic and Hygienic Treatment .—Detailed attention 
should be paid to the correction of all dietetic errors that 
may seem causative of the disorder. As regards diet, the 
experience of each patient should be regarded, and care 
should be taken not to exclude too many articles of food, 
on account of the danger of undermining the general health. 
Over-eating, on the other hand, should be avoided. As a 
general rule, pastries, sweets, hot breads, and fried foods 
29 


450 MANUAL OF THE PRACTICE OF MEDICINE. 

should be excluded from the diet, and tea and stimulants 
are to be allowed only in moderation. Starches and sugars 
should be limited in cases with marked flatulence. The 
patient should not eat too hurriedly, nor should he eat 
heartily when too tired to digest properly, nor indulge in 
severe exercise after a full meal. Nibbling between meals 
and at night should not be permitted. Food difficult to 
digest, such as pork, hard-boiled eggs, young veal, and 
cabbage, should be avoided, and too much ice-water is not 
to be taken during the meals. Careful attention should be 
paid to the maintenance of good general health. The 
patient should have sufficient sleep, exercise, and fresh air. 
Anaemic and weakly conditions should be combated by 
appropriate medication. Strychnine is often of the greatest 
service in increasing the nervous and motor power of the 
stomach. Change of air and occupation and travel will fre¬ 
quently do more than all medicines combined. 

2. Medicinal Treatment .—The indications are to increase 
digestive power and to check fermentation. To obtain the 
best results the patient should be watched and the effect of 
diet be observed. If there be difficulty in digesting the 
albuminoids, dilute hydrochloric acid and pepsin aie indi¬ 
cated. The dilute acid is to be given in 15-to 20-drop 
doses after meals 5 and it is important in the use of pepsin 
to find a preparation that has actual digestive value, as most 
of the preparations in the market are worthless. Fairchild s 
essence of pepsin in 5 _ drop does is to be recommended. 
Pancreatin in doses of from 5 to 15 grains, with an equal 
amount of bicarbonate of soda, may be given one or two 
hours after meals ; or tablets of pepsin and pancreatin in 
combination, although objectionable for theoietical reasons, 
may be given with benefit. Papoid in 1- or 2-grain doses 
may be given in tablets after meals 5 this diug has the ad¬ 
vantage, as has pancreatin to a less extent, of digesting 




CHRONIC CATARRHAL GASTRITIS. 45 I 

both albumins and starches. If there be difficulty in 
digesting the starches, pancreatin or papoid may be used, 
or diastase may be given, especially if the stomach-contents 
be excessively acid. A teaspoonful of Forbes’s diastase 
before meals acts efficiently in such cases. 

Glandular activity of the stomach may be stimulated by 
the bitter tonics, quassia, gentian, columbo, cardamom, and 
condurango, preferably combined with alkalies and given 
well diluted before meals. This form of treatment is often 
of the greatest value. 

fermentation and flatulence may be controlled by atten¬ 
tion to the diet and by the use of the preceding remedies. 
In obstinate cases antiseptics may be given after meals. 
Creosote, thymol, the essential oils, bismuth subgallate or 
salicylate, naphthaline, hydro-naphthol, and salicylate of 
sodium or salol may be used. The best results in the 
writer’s hands have followed creosote (Tfljij-iv) and sub¬ 
gallate of bismuth (gr. v-x) after meals. 

If there be much mucus, especially in obstinate cases, 
systematic lavage should be resorted to. The stomach 
should be washed out every day or every second day, pref¬ 
erably the last thing at night or early in the morning, when 
the stomach is empty. A weak solution (2 per cent.) of 
bicarbonate of sodium or of boric acid may be employed 
in the more aggravated cases. Patients soon learn to wash 
out their own stomachs, and they are usually much pleased 
with the results. In cases not severe enough to demand 
lavage much good can be accomplished by drinking one or 
two glasses of hot water half an hour before breakfast, and 
possibly before each meal. Hot alkaline waters are even 
more effective. After drinking the hot water the patient 
should lie down for a quarter of an hour, if possible, on the 
right side. The bowels should be kept regular, and an 
occasional mercurial is often beneficial. 


452 MANUAL OF THE PRACTICE OF MEDICINE. 

Distressing symptoms should receive appropriate treat¬ 
ment. Vomiting is rarely troublesome except in children. 
It may be controlled by bismuth, oxalate of cerium, creosote, 
drop doses of carbolic acid, nitrate of silver, dilute hydro¬ 
cyanic acid in 2-drop doses, and chloroform. Acidity may 
be relieved temporarily by soda or magnesia. 

DILATATION OP THE STOMACH; GASTRECTASIS. 

Etiology.—The causes of dilatation of the stomach may 
be divided into three groups : 

1. Mechanical obstruction of the pylorus from cancerous or 
cicatricial stenosis, from hypertrophy of the connective and 
muscular tissues, from congenital narrowing, from external 
pressure of a tumor, or from floating kidney. It should be 
remembered that stenosis may exist without dilatation, the 
stenosis being compensated by hypertrophy of the muscular 
coats. 

2. Abnormalities in the contents of the stomach. Excessive 
eating and drinking may cause dilatation ; such cases are 
common among insane and diabetic patients and among 
workmen in breweries who drink large quantities of beer. 
In rare cases acute dilatation has occurred from this cause. 
Fermentation of food generates gases which press upon and 
stretch the gastric wall, especially if it be weakened by 
inflammation. 

3. Impairment of muscular force. This condition may 
occur with partial destruction of the gastric wall, as in can¬ 
cer or ulcer; with chronic gastritis, especially the atro¬ 
phic and sclerotic forms; with peritoneal adhesions; and 
with adynamic states of the general system, such as general 
debility, anaemia, tuberculosis, rickets, and illnesses of all 
kinds. 

Pathology.—The various causes cited operate in one 
way—to cause a habitual increase of stomach-contents. 


DILATATION' OF THE STOMACH. 


453 


More food being put into the stomach than can conveni¬ 
ently pass the pylorus, the stomach becomes gradually 
dilated, so that it may reach an enormous size. In moder¬ 
ate cases the lower border of the viscus reaches the um¬ 
bilicus, while in advanced cases it lies on the level of the 
anterior superior spines or even dips into the pelvis. If 
stenosis of the pylorus exists, the muscular tissue may be 
hypertrophied. The mucous membrane regularly shows 
the lesions of chronic catarrhal gastritis. 

Symptoms.—Symptoms due to the primary cause often 
precede those due to the dilatation. The symptoms of 
chronic gastritis are present in every case, associated with 
the more characteristic symptoms of dilatation. Of these 
symptoms vomiting is the most characteristic. At intervals 
there is vomited a large quantity of liquid and food, as much 
as three or four quarts being vomited at one time. The 
vomita, which are sour from the presence of fatty acids, 
although HC 1 is diminished or absent, consist of undigested 
fermenting food and mucus often containing bacteria, yeast 
fungi, or sarcinae ventriculi. On standing, the vomita sepa¬ 
rate into three layers: an upper, of a brownish froth ; a middle, 
of a turbid fluid ; and an under layer of food and debris. It 
is diagnostic for the patient habitually to vomit food taken 
the day previous. According to the size of the stomach 
and the degree of pyloric stenosis allowing more or less of 
the gastric contents to escape into the intestine, the stomach 
will be more or less rapidly over-filled with food and drink, 
and the consequent disengorgement leads to a certain peri¬ 
odicity in the vomiting. In very bad cases the stomach may 
toward the close of the disease lose its contractile power, 
so that vomiting ceases; this sign is to be regarded as of 
serious import. 

Heartburn and acid eructations are frequent, from the 
fermentation of retained undigested food. There may be 


454 MANUAL OF THE PRACTICE OF MEDICINE. 

dragging feelings and a sense of weight from the mechanical 
effects of the dilatation. Pain and oppression are commonly 
observed. The bowels are usually constipated, although 
attacks of colicky pain and diarrhoea may occur, from the 
passage of the acid fermenting food into the intestine. 

If stenosis of the pylorus is marked, little food or fluid 
may pass the obstruction. In consequence, loss of flesh 
and of strength become apparent, the patient is unnaturally 
hungry and thirsty, the urine becomes diminished in quan¬ 
tity and is concentrated, and painful cramps of the muscles 
may occur. 

Physical Signs.— Inspection .—The abdomen is large and 
bulging, and the position of the greater curvature may be 
seen. In cases with pyloric stenosis waves of peristalsis or 
of antiperistalsis may be seen. 

Palpation often reveals the peristalsis. If there be ste¬ 
nosis of the pylorus from simple or cancerous thickening, 
the mass may be detected. In many cases the boundaries 
of the stomach may be appreciated, the feeling of resistance 
being compared to that of an air-cushion. Bimanual palpa¬ 
tion may elicit splashing sounds. These sounds, which are 
caused by the shaking together of air and water, may often 
be elicited in a healthy stomach after eating. To be of any 
diagnostic value, the splashing should be produced when 
the normal stomach should be empty—two hours after 
drinking, seven hours after a general meal. To facilitate 
palpation the stomach may be inflated. This should always 
be done with caution, and never to an extreme degree, espe¬ 
cially if cancer or ulcer be supposedly present. The 
patient may be given gr. xx-3j of bicarbonate of sodium, 
followed by an equal amount of tartaric acid in water, and 
the inflated stomach can then usually be felt distinctly. A 
stomach-tube should be at hand for the withdrawal of the 
gas, should unpleasant symptoms occur. Another method 


DILATATION OF THE STOMACH. 


455 


is by passing a stomach-tube and pumping air through it 
by a Davidson syringe. The introduction of a stiff bougie 
so that its point can be felt through the abdominal wall is 
not a justifiable procedure. 

Percussion .—The patient standing upright, two zones are 
to be distinguished—an upper zone of hyper-resonance, and 
a lower zone of dulness. If this dull zone be at or below 
the level of the umbilicus, dilatation may be suspected. To 
prove that the dulness is due to the presence of food or of 
fluid in the stomach, and not in the colon, the stomach may 
be siphoned of its contents, with the disappearance of the 
dulness. 

It is important to remember that in women with lax 
abdominal walls the whole stomach may be displaced down¬ 
ward without being increased in size. 

Auscultation .—Succussion is readily elicited, and a fine 
sizzling sound is frequently heard. 

The prognosis in mild cases not due to pyloric stenosis 
is fairly good, a large number of cases being entirely cured, 
while in others the disease does not progress. If due to 
stenosis of the pylorus, the prognosis is bad, depending 
upon the extent and nature of the stenosis. 

Treatment.—Attention to the diet is of the first import¬ 
ance, and without it neither a cure nor an improvement can 
be expected. The food should be simple, concentrated, 
and easily digested, and in bad cases should be taken in 
small quantities at frequent intervals. Carbohydrates and 
fatty food should be permitted only in the smallest amount, 
and liquids are to be partaken of sparingly. In advanced 
cases a resort to predigested foods and peptones for short 
periods is often of service. A cup of hot water before 
meals will allay excessive thirst more effectively than a 
larger amount taken with or after the meals. To relieve 
the dilated stomach of its accumulated contents the stomach 


456 MANUAL OF THE PRACTICE OF MEDICINE. 

should be emptied and then be washed clean with warm 
water or with weak alkaline solutions. If fermentation be 
active, a I per cent, solution of salicylic acid or of resorcin 
may be used. Lavage should be practised the last thing 
at night or early in the morning, and it should be repeated 
every day or every second day, according to the require¬ 
ments of the case. By systematic lavage not only is the 
weight of the accumulated food removed, but the stomach 
is relieved of mucus and the irritating fatty acids of ferment¬ 
ing food, and the absorbent and secretory functions are 
stimulated. Strychnine is of great value, through its power 
to restore tone to debilitated muscular fibre; it is of special 
service in dilatation not depending upon pyloric obstruc¬ 
tion. Iron and tonics are indicated to restore general sys¬ 
temic tone. Pepsin, papoids, pancreatin, and hydrochloric 
acid may be employed as digestive aids ; antiseptics are use¬ 
ful if fermentation be active. 

Faradization, either through the abdominal wall or by an 
electrode introduced through a stomach-tube, has been rec¬ 
ommended. Massage from the fundus toward the pylorus 
is often beneficial. It should be employed daily, five hours 
after the principal meal. If there be bulging of the epigas¬ 
trium, a cushion, a pad, or an elastic abdominal bandage 
should be worn. 

In cases of stenosis of the pylorus operative procedures 
are often indicated. Gastro-enterostomy may be performed. 
In case the stenosis be cicatricial, Loreta’s operation of 
stretching the pyloric ring, which has been followed by 
good results in the majority of cases, may be performed. 

ULCER OF THE STOMACH. 

Etiology and Synonym.—Ulcer of the stomach is found 
at post-mortems more frequently than it is diagnosed during 
the life of the patient, ulcer, either cicatrized or open, being 


ULCER OF THE STOMACH 


45 ; 

found in 5 per cent, of persons dying from all causes, the 
scais being the more common. Females are more fre¬ 
quently affected than males, in the proportion of 3 : 2. 
The gieatest liability is between the ages of twenty and 
forty years, but the disease is not uncommon up to the age 
of sixty. It iaiely occurs in young children. It is more 
common in anaemic and chlorotic patients and those with 
mensti ual disorders, and it is not infrequently associated 
with tuberculosis. It occurs especially among servant-girls 
and in shoemakers, in the latter case being consequent, pos¬ 
sibly, upon the pressure on the stomach while at work. It 
is not as common in America as in Europe. Synonym: 
Peptic ulcer. 

Pathology. —There is but one ulcer in 80 per cent, of 
all cases, but as many as 34 ulcers have been found. The 
usual situation (86 per cent.) is on the posterior wall near 
the pylorus, close to the lesser curvature. The ulcers vary 
in diameter from one-half to two inches, although they 
may be much larger. The usual shape is round or oval, 
although the larger ulcers are apt to be irregular, and 
several ulcers may coalesce to form one of an irregular 
shape. The ulcer has an oblique funnel shape, becoming 
smaller as it extends deeper, the successive ulcerated coats 
being distinctly terraced. The floor has a clean, “ punched 
out ’ appearance, free from inflammatory changes, but in old 
cases the floor and walls of the ulcer may be indurated 
and thickened. I he depth varies, the ulcer sometimes in¬ 
volving only the mucous coat, at other times extending 
to the deeper structures and even perforating the stomach- 
wall. The mucous membrane of the stomach shows almost 
regularly the lesions of a subacute or chronic catarrhal gas¬ 
tritis. Changes in the blood-vessels of the stomach have 
been found in a large proportion of cases. Among these 
changes may be mentioned embolism, thrombosis, and dif- 


458 MANUAL OF THE PRACTICE OF MEDICINE . 

fuse endarteritis of the arteries supplying the ulcerated area. 
Small aneurysms have been found in the floor of the ulcer. 
The mucous membrane of the stomach may show the 
lesions of subacute or chronic catarrhal gastritis. 

Sequelae and Complications of Ulcer.—These compli¬ 
cations are of the utmost importance. 

1. The ulcer may cicatrize. In some cases hardly any 
scar is left; in other cases, especially if extensive ulcera¬ 
tion of the muscular coat has occurred, considerable puck¬ 
ering or deformity may occur. Cicatricial stenosis of the 
pylorus with dilatation of the stomach is a not infrequent 
result. It often happens that large ulcers may remain open 
for years without showing signs of healing. 

2. The ulcer may perforate the wall of the stomach. 
Gastric contents enter the peritoneum, and a rapidly fatal 
peritoneal septicaemia follows. Perforation, which occurs 
in 6 per cent, of all cases, is more common with ulcers of 
the anterior than with those of the posterior wall. 

3. Adhesions may form between the stomach and the 
surrounding viscera, especially the left lobe of the liver, the 
pancreas, and the omental tissues, nature “ putting a patch 
on ” to reinforce the weakened spot and to prevent perfora¬ 
tion. Extension of the ulceration and secondary infection 
of pus microbes may lead to fistulous tracts and suppu¬ 
rating cavities in these adhering organs. Gastro-intestinal 
fistulse are thus formed, and perforation into the pleura, the 
pericardium, and the left ventricle of the heart has been 
known to occur. The suppurative process may extend 
along the veins, causing a suppurative pylephlebitis with 
multiple abscesses in the liver. The adhesions may not be 
extensive enough to prevent perforation, but may suffice to 
shut the site of rupture from the general peritoneal cavity, 
so that a localized peritoneal abscess results. Perforation 
of the posterior wall produces an air-containing abscess in 


ULCER OF THE STOMACH. 459 

the lesser peritoneal cavity, known as “ subphrenic pyo¬ 
pneumothorax.” 

4. Erosion of a blood-vessel is of common occurrence. 
This accident may occur with recent acute ulcers, but it is 
more common in the chronic form with spreading ulceration. 
Ulcers on the posterior wall of the stomach may erode the 
splenic artery or the artery of the lesser curve. 

Pathogenesis.—All authorities agree that gastric ulcer 
results from self-digestion of part of the stomach-wall by 
the gastric juice. Self-digestion is prevented in the normal 
stomach by the circulation of alkaline blood in the gastric 
mucous membrane. Aside from this, not much is known. 
The common occurrence of ulcer with anaemia and chlo¬ 
rosis, in which diseases a diminished alkalescence of the 
blood is present, would suggest that diminished alkalinity 
allowed of self-digestion; but this theory has serious objec¬ 
tions. The generally accepted theory is that for some 
reason the circulation stagnates in a certain area of the 
stomach-wall, and, its nutrition failing, the part is acted upon 
and destroyed by the gastric juice. Experimental embol¬ 
ism of the gastric arteries has been followed by ulceration, 
and this experimental evidence accords with the funnel 
shape of the ulcer and with the actual post-mortem dem¬ 
onstration of an embolus or a thrombus plugging the 
nutrient artery in some cases. Local pressure or trauma¬ 
tism is supposed to act locally to produce changes in the 
circulation. Talma lately suggested that a cramp-like con¬ 
traction of the stomach on full contents may cause such 
pressure on its wall as to interfere with the circulation and 
to allow of ulceration. By filling the stomach of an animal 
with gastric juice and ligating the orifice he found that, by 
causing firm contractions with faradism, ulcers resulted. 

The formation of ulcers seems to be favored by hyper¬ 
acidity and hypersecretion. 


460 MANUAL OF THE PRACTICE OF MEDICINE. 


Symptoms.—There may be any or all of the symptoms 
of chronic gastritis. These dyspeptic symptoms may be 
trifling or of the most aggravated character, but to some 
extent they are almost invariably present. The distinctive 
symptoms are pain and tenderness, vomiting, and the vom¬ 
iting of blood. 

Pain is the most constant symptom. The characteristic 
pain is sharply localized in the epigastrium, frequently run¬ 
ning through to the back. It is brought on by eating, usu¬ 
ally within a few minutes, and it is aggravated by irritating 
food or by an excessive quantity of food. It ceases when 
the stomach is relieved of its contents either by the normal 
exit of food through the pylorus or by the act of vomiting. 
The pain is increased by exercise and is diminished by rest. 
There is usually a localized area of tenderness an inch 
or so below the ensiform cartilage. There may be, how¬ 
ever, relief from pressure on the epigastrium. In many 
cases this classical pain is not present, variations being 
common. 

(a) In some cases there is the ordinary pain of an asso¬ 
ciated gastritis. 

(b) In other cases the pain does not occur until two or 
three hours after eating or until the stomach is empty ; the 
pain, being due to hyperacidity, is relieved by food. 

( c ) In some cases the pain comes on in attacks at in¬ 
tervals for weeks or months, and then the patient goes for 
a long time without attacks; the pains, however, return 
after a variable leno-th of time. 

o 

( d ) In other cases the pain is reflected to the nerves of 
the abdominal wall and has the characters of a neuralgia. 

Vomiting .—The characteristic of the vomiting rests not 
with the act itself, but in the relief it gives to the pain. A 
pain after eating, vomiting, and relief is the regular sequence. 

The vomited matters, which consist of undigested food, 


ULCER OF THE STOMACH 461 

usually without evidences of fermentation, generally contain 
HC1 in more than the normal quantity. 

The vomiting with ulcer is not constant, and when it 
does occur it varies greatly in severity, some patients vom¬ 
iting nearly everything they eat, others vomiting but sel¬ 
dom, if at all. In other cases the vomiting is due to the 
associated gastritis. 

Vomiting of blood occurs in about one-half the cases. 
The vomiting may be slight, but more commonly it is pro¬ 
fuse. If profuse and sudden, the blood raised is red, partly 
clotted, and unaltered. If less profuse, it may be retained 
in the stomach for a longer time, so that by alteration by 
the gastric juice it becomes black or brown, resembling 
“ coffee-grounds.” Repeated hemorrhages lead to a high 
grade of anaemia; sudden profuse hemorrhage may cause 
death. In most cases some blood, and in rare cases all the 
blood, passes the pylorus and is evacuated with the stools, 
giving them a black, tarry appearance. On adding water to 
these stools a more characteristic blood-color is developed. 

In old ulcers with a thickened base an indurated mass 
may be felt on examination in the neighborhood of the 
pylorus. In these cases the symptons of dilatation of the 
stomach may be present. 

Hysterical and anaemic symptoms are often present; fre¬ 
quently they may so overshadow the symptoms of the ulcer 
that the latter condition is overlooked. 

Varieties in Clinical Course.— 1. In some cases the dis¬ 
ease runs a latent course and is found after death from some 
other disease, without having given symptoms during life. 

2. Some cases run a latent course until there occurs a 
profuse hemorrhage which may terminate fatally or which 
may be followed by the symptoms of chronic ulcer. 

3. With or without a brief history of gastric disturbance, 
sudden perforation occurs, causing speedy death. 


462 MANUAL OF THE PRACTICE OF MEDICINE. 

4. In some cases the characteristic symptoms are not 
marked, but resemble those of chronic gastritis, so that a 
diagnosis cannot with certainty be made. 

5. In some patients the disease shows periods of appar¬ 
ent cure, after which there is a return of the symptoms. 
It is hard to say whether fresh ulcers form or whether the 
cicatrix of an old ulcer becomes ulcerated. 

6. In some cases the anaemia and cachexia from malnu¬ 
trition become so marked as to suggest pernicious anaemia 
or cancer. 

7. In other cases the symptoms of pyloric stenosis and 
secondary dilatation of the stomach are so marked that the 
symptoms of the primary ulcer are overlooked. 

The prognosis is uncertain, as a fatal hemorrhage or 
perforation may occur at any time. The possibility of 
fistulae and suppuration without the stomach, as noted 
under the heading of “ Pathology,” should be kept in 
mind. The duration of the disease varies from a few 
months to a number of years, the average being from three 
to five years. Relapses are frequent. Recent ulcers are 
more amenable to treatment than old, indurated ulcers. 
Death from hemorrhage occurs in 4 per cent, of all cases ; 
from perforation, in 6.5 per cent. About 15 per cent, of 
all cases of ulcer of the stomach are fatal. 

It is often hard to tell when the symptoms of ulcer end, 
as gastritis, neuralgia, or dilatation of the stomach due to 
the presence of the cicatrix may continue gastric symp¬ 
toms. 

Treatment consists in rest, attention to the diet, and the 
administration of drugs. 

When the diagnosis is made, absolute rest in bed should 
be enforced until acute symptoms have subsided. The 
more absolute the rest the better the results. In chronic 
cases modifications of the rest-cure are permissible. 


ULCER OF THE STOMACH. 


4^3 


The diet should be regulated carefully and systematically. 
The food should be bland, easily digestible, and taken in 
small quantities at frequent intervals. The diet and rest 
should continue for at least three months. Milk (which 
may be peptonized), eggs, rice, sweetbreads, beef extracts, 
and milk gruel may be given at the start, with scraped beef, 
young chicken, and farinaceous puddings after a time. In 
very severe cases rectal alimentation should be resorted to 
for a few days, after which time it may be used to supple¬ 
ment feeding by the mouth. 

Medicinal Treatment .—Lavage with weak alkaline solu¬ 
tions is serviceable in cases with hyperacidity, especially if 
vomiting be marked. It is also of benefit should gastritis 
or dilatation add its symptoms. 

For the gastritis the ordinary methods of treating this 
condition may be tried. 

For the pain, bismuth, oxalate of cerium, Hoffmann’s 
anodyne, or dilute hydrocyanic acid may be used. Cold or 
hot applications to the epigastrium or counter-irritation by 
iodine, by blistering, or by a nitric-acid issue may be em¬ 
ployed. Morphine is to be withheld because of the danger 
of forming the habit. If the pain be due to hyperacidity, 
alkalies with cannabis indica may be employed, and the 
stomach is to be washed out. If the pain be due to gas¬ 
tritis, lavage and antiseptics will frequently relieve it. 

Vomiting is to be controlled by systematic lavage, by the 
use of bismuth, oxalate of cerium, and hydrocyanic acid, 
and by regulation of the diet. In severe cases rectal ali¬ 
mentation should be resorted to. 

Haematemesis is to be treated with absolute rest and quiet 
of body and mind and by the giving of cracked ice. The 
patient should be put as rapidly as possible under the influ¬ 
ence of opium, preferably by hypodermics. Drugs by the 
mouth, such as gallic acid, ergot, and acetate of lead, are 





464 MANUAL OF THE PRACTICE OF MEDICINE . 

of no service, and the efficacy of local applications of ice 
is doubtful. Stimulation should be moderate, as a depressed 
state of the circulation is nature’s method of checking hem¬ 
orrhage by allowing the formation of a thrombus. 

After hemorrhage all food should be withheld from the 
stomach for several days. 

Anaemic and cachectic conditions should be treated 
steadily and persistently by iron, arsenic, good fresh air, 
and a change of climate or of occupation if necessary. 

CANCER OF THE STOMACH. 

Etiology. —Next to the uterus, the stomach is the most 
frequent seat of primary cancer, the organ being involved in 

21.4 per cent, of a total of over 30,000 cases. According to 
Welch, cancer of the stomach is the cause of death in 1 per 
cent, of all persons dying after the age of twenty years. It 
is almost always primary. The actual cause of cancer of the 
stomach is not understood. It occurs in men a little more fre¬ 
quently than in women, and it is more common in some races 
than in others, pure-blooded negroes being comparatively ex¬ 
empt. Three-fourths of all cases occur between the fortieth 
and seventieth years, but the occurrence of cancer between 
the ages of twenty-five and forty is not as exceptional as is 
often represented. The influence of heredity is seen in 14 
per cent, of all cases. Chronic gastritis has preceded cancer 
in a fair number of cases, and carcinomatous changes in 
the wall of an old gastric ulcer have been described. 

Pathology. —The varieties met with, in the order of fre¬ 
quency, are cylindrical-celled epithelioma, encephaloid, scir¬ 
rhous, and colloid cancer. According to Welch, the pyloric 
region is involved in 60.8 per cent., the lesser curvature in 

11.4 per cent., the cardiac end in 8 per cent., the posterior 
wall in 5.2 per cent., the whole or the quarter part of the 
stomach in 4.7 per cent., multiple tumors 3.5 per cent., 


CANCER OF THE STOMACH. 465 

greater curvature in 2.6 per cent., anterior wall in 2.3 per 
cent., fundus in 1.5 per cent. 

Cancer begins in the mucous membrane of the stomach 
and grows in all directions. The portion of the growth 
projecting into the cavity of the stomach may be broad and 
flat or cauliflower-like, or ulceration may occur, allowing 
of hemorrhage or of perforation. Perforation into the peri¬ 
toneum occurs in 4 per cent, of all cases, being usually pre¬ 
vented by the formation of adhesions between the stomach 
and adjacent structures. More rarely perforation occurs 
into the colon or through the abdominal wall, or fistulae 
may be formed into the lungs, the pleura, and the small 
intestine. Ulceration is most common with encephaloid 
and cylindrical-celled epithelioma, less frequently in scir¬ 
rhous and colloid cancer. Growths about the pylorus are 
apt to cause pyloric stenosis with secondary dilatation of 
the stomach. Growths in the cardia are apt to cause stenosis 
and secondary dilatation of the oesophagus. Chronic catar¬ 
rhal gastritis almost invariably occurs with the growth of 
cancer. 

Encephaloid cancer grows rapidly and forms cauliflower¬ 
like masses projecting into the cavity of the stomach, tend¬ 
ing to ulcerate easily. It is soft, of a grayish-white or 
reddish-white color, and contains much blood. Micro¬ 
scopically the growth consists of a scanty stroma enclosing 
alveoli filled with irregular polyhedral and cylindrical cells. 
Metastases are common. 

Cylindrical-celled epithelioma somewhat resembles the 
encephaloid, but is firmer, especially at the edges. It is 
prone to ulcerate and to form metastases. Cysts contain¬ 
ing mucus are often found. This form of tumor consists of 
elongated tubular spaces filled with columnar epithelium 
with an abundant stroma, and it resembles the structure 
of tubular glands. 


30 


466 MANUAL OF THE PRACTICE OF MEDICINE. 

Scirrhous cancer may occur as a hard, circumscribed 
tumor or as a diffused thickening of the gastric wall. It 
is hard to the feel, and it is most often found at the pylorus, 
causing stenosis. Scirrhus has but little tendency to ulcer¬ 
ate. It consists of a hard fibrous stroma with relatively few 
and small alveoli. 

Colloid cancer shows itself as an extensive uniform infil¬ 
tration and thickening of all the layers of the wall of the 
stomach. It spreads with great frequency to involve adja¬ 
cent structures, although actual metastasis is comparatively 
rare. It shows trabeculae of connective tissue enclosing 
large alveoli filled with translucent colloid material. To 
this variety the name of “ alveolar cancer ” has been ap¬ 
plied. 

These varieties are often mixed in the same specimen, so 
that it is hard to say in what class the growth is to be placed. 

Secondary cancerous growths occur by (i) direct exten¬ 
sion, involving the oesophagus or any structure to which 
the stomach may become adherent, or by (2) metastasis. 
This latter is most frequent in the lymphatic glands in the 
neighborhood of the stomach ; next in frequency in the 
liver, the peritoneum, the omentum, and the intestines ; less 
frequently in the pleura and the lungs. The liver is involved 
in about one-third of all cases. The cervical and inguinal 
lymphatic glands are not infrequently involved, and occa¬ 
sionally growths occur subcutaneously near or at the navel. 

The symptoms of cancer of the stomach may be de¬ 
scribed as gastric, constitutional, and those due to the sec¬ 
ondary growths. 

Gastric Symptoms. — (a) As chronic gastritis almost inva¬ 
riably accompanies cancer of the stomach, it gives rise to 
any or all of its regular symptoms. The appetite is usually 
more completely lost than in uncomplicated gastritis. 

(h) Pain occurs in 92 per cent, of all cases, being rarely 


CANCER OF THE STOMACH 467 

absent except in old people. The pain is severe, more or 
less continuous, and is described as burning, gnawing, or 
neuralgic. It may be referred to the epigastrium or be¬ 
tween the scapulae, but the locality of the pain is no indi¬ 
cation of the seat of the growth. Pain is usually increased 
by eating, although this may not be evident until some little 
time after taking food. 

The pain differs from the typical pain of ulcer (1) in be¬ 
ing more continuous, so that the patient is often awakened 
at night by it; (2) in being less dependent on food; (3) in 
the increased pain being delayed some little time after tak¬ 
ing food; (4) in being less sharply localized; and (5) in not 
usually being relieved by vomiting. There is generally ten¬ 
derness on pressure over the growth, but the tenderness is 
less marked and less sharply localized than in ulcer. 

(c) Vomiting occurs in from 80 to 88 per cent, of all 
cases. As a rule, it does not appear until the latter part 
of the disease, when the cancer has attained a considerable 
size, whereas the vomiting of ulcer comes on early. Vom¬ 
iting is more frequent if either orifice be involved. If the 
pylorus be affected, vomiting occurs longer after eating 
than if the cardiac orifice be involved, the food often re¬ 
maining for some hours in the stomach without being 
digested. There are cases, however, in which vomiting is 
an early and a distressing symptom, severe enough to cause 
a fatal termination. If the stomach be dilated, the vomit¬ 
ing may be typical of that condition. The vomited matters 
consist of undigested food, often fermenting and mixed with 
mucus. Fragments of ulcerating growths may be found, 
establishing a diagnosis. These fragments, however, are 
more frequently found in the washing out of the stomach. 
Free hydrochloric acid is absent in the great majority of 
cases of cancer of the stomach. As it is so frequently 
absent in other conditions, such as atrophy of the gastric 


468 MANUAL OF THE PRACTICE OF MEDICINE. 

mucous membrane, its absence is not diagnostic, but is 
merely corroborative if other symptoms of cancer be pres¬ 
ent. Its presence, however, is strong presumptive, although 
not absolute, evidence that cancer does not exist. To test 
for HC 1 , Ewald’s test-breakfast, consisting of a Vienna roll 
and a cup of weak tea without milk or sugai, should be 
given on a fasting stomach. In one houi a soft stomach- 
tube should be passed and the gastic contents be expressed 
with gentle pressure over the stomach. After filtering, a 
drop of Gunzberg’s reagent should be added to each cubic 
centimeter of the filtrate. If HC 1 be present, a cherry-red 
color is developed and cherry-red crystals are precipitated. 
Gunzberg’s reagent, or the phloroglucin-vanillin test, con¬ 
sists of— 

Phloroglucin, 2 grams; 

Vanillin, I gram ; 

Absolute alcohol, 3 ° grams. 

This liquid is yellow in color and should be kept in a dark 
bottle not exposed to the light. This test does not react 
to lactic acid. 

(d) Hemorrhages .—It is important to distinguish between 
the slight and the copious hemorrhage of gastric cancer. 
An admixture of a small quantity of blood with the vomit 
is present in about half the cases. The blood is brown or 
black, resembling coffee-grounds, the normal pigment hav¬ 
ing been converted by the acids of the stomach into dark- 
brown haematin. 

Copious hemorrhages occur in about one-eighth of the 
cases. The blood may be bright red or more or less dark¬ 
ened, according to the length of time it has been retained 
in the stomach. Following profuse haematemesis some 
black tarry blood is usually passed with the stools. 

Hemorrhage in cancer differs from that in ulcer (i) in 


CANCER OF THE STOMACH. 


469 

being more frequent; (2) in being usually less copious ; (3) 
in being retained longer in the stomach, with the conse¬ 
quent coffee-ground appearance; and (4) in occurring in 
the latei stages, when the cancer is ulcerating and the 
patient is emaciateo and cachectic, whereas in ulcer the 
hemorrhage is an early symptom, occurring when the 
patient is apparently in good health. 

(e) If dilatation of the stomach or stenosis of the cardiac 
end of the oesophagus complicate, the symptoms of these 
conditions will be added. 

Constitutional Symptoms .—The patient grows progres¬ 
sively anaemic, developing a waxy or “beeswax” pallor 
which is quite characteristic; emaciation and prostration 
become more and more marked; there may be a slight 
irregular rise in the afternoon temperature. Slight oedema 
of the ankles is common, and a general itching of the skin 
is complained of—a symptom which in old people should 
suggest cancer or diabetes. In rare cases chills with par¬ 
oxysmal elevations in temperature have been recorded. 
Delirium or coma may occur as a terminal event. 

Symptoms of the secondary growths vary according to 
their size and location. Metastases in the liver cause a 
general enlargement of that organ, with pain, tenderness, 
and jaundice. Ascites is not uncommon. Involvement 
of the peritoneum and the omentum gives rise to ascites 
and abdominal pain and tenderness, and on examination 
the thickened masses may be evident. The glands above 
the clavicle are often enlarged. The subcutaneous nodules 
near the umbilicus have been alluded to. 

Physical Examination.—Owing to the position of the 
stomach, only tumors of the pylorus, of the anterior wall, 
and of a large part of the greater curvature are accessible 
to examination. Tumors of the fundus, of the posterior 
wall, and of the greater part of the lesser curvature cannot 


470 MANUAL OF THE PRACTICE OF MEDICINE. 

be detected unless of some considerable size or unless the 
stomach be displaced downward. Tumors of the cardiac 
end cannot be detected at all. 

As the growth is usually at or near the pylorus, the 
tumor is in most cases felt in the epigastric region as a 
firm, hard, nodular mass, tender on pressure. It is not in¬ 
fluenced by respiration unless adhesions with the liver are 
present. Owing to the weight of the growth dragging the 
pylorus downward, the tumor may be felt as low down as 
the iliac region. A definite tumor is felt in 80 per cent, of 
all cases. Examination may be made with the patient lying 
down, with the knees drawn up so as to relax the abdominal 
wall; in doubtful cases examination in the knee-chest 
position may be more satisfactory. Inflation of the stom¬ 
ach with gas (see Dilatation of the Stomach) may be re¬ 
sorted to; this procedure frequently brings the tumor 
into reach. In cases of colloid cancer no regular tumor- 
mass may be felt, but the stomach-wall feels abnormally 
thick and resistant. It is rare to feel a tumor before the 
third to the sixth month of the disease. 

Peculiarities in the Clinical Course.— I. Some cases 
run a latent course, death resulting from some intercurrent 
disease. This occurs especially in aged subjects. 

2. In some cases gastric symptoms may be insignificant, 
while anaemic and cachectic symptoms are marked. These 
cases are often diagnosed as pernicious anaemia or Bright’s 
disease. 

3. In other cases gastric symptoms are developed, but 
are not characteristic. These cases are often diagnosed as 
chronic gastritis or dilatation. 

4. There are cases in which the symptoms of the primary 
gastric cancer are obscured by symptoms arising from the 
secondary growths. These cases are then diagnosed as 
primary cancer of the liver or of the peritoneum. 


NON-CANCEROUS TUMORS OF THE STOMACH. 471 

The prognosis is practically hopeless. The duration of 
the disease is usually about two years. Cases live about 
one year after the diagnosis is made. Occasionally may 
be seen cases with a rapid course terminating in from three 
to six months. 

Treatment.—If the growth be localized and non-adhe¬ 
rent to other structures, and if no secondary deposits are 
present, surgical interference may be justifiable. Resection 
or gastro-enterostomy may be performed, although the re¬ 
sults as yet are far from encouraging. Medicinal treatment, 
on the other hand, is merely palliative. Condurango at one 
time was lauded as a specific, but it is now recognized only 
as an excellent stomachic tonic, in some cases relieving the 
pain and the vomiting. It may be given as a decoction, a 
wine, or a fluid extract. Hydrochloric acid is indicated as 
an aid to digestion, and it is usually of service. The pain 
and the vomiting are to be controlled on general principles 
of treatment. As the disease is certainly fatal, there can 
be no objection to giving opium, as it makes no difference 
whether or not the habit is formed. 

NON-CANCEROUS TUMORS OF THE STOMACH. 

These growths are rare and are not causative of destruc¬ 
tive symptoms. 

Polypi are the most common form. They are composed 
of hypertrophied mucous membrane, are rarely larger than 
a bean, and are usually multiple. 

Sarcomata are rare. Fibromata and lipomata are occa¬ 
sionally met with. Lymphomata may be found in connec¬ 
tion with leukaemia or pseudo-leukaemia. Myomata or ftbro- 
myomata may occur in the form of large polypi. Cases of 
foreign bodies have often been mistaken for tumors. The 
most remarkable instances are the hair balls in hysterical 
women who are in the habit of eating their own hair. 


472 MANUAL OF THE PRACTICE OF MEDICINE. 


HEMORRHAGE FROM THE STOMACH. 

Synonyms.—Haematemesis ; Gastrorrhagia. 

Etiology.—The causes of hemorrhage from the stomach 
are exceedingly various ; they may be grouped as follows: 

1. Traumatism. —( a ) Mechanical injuries, as blows or 
falls ; penetrating wounds or the rough introduction of a 
stiff stomach-tube, (b) Chemical injuries by strong acids or 
alkalies or by corrosives. 

2. Local Disease of the Stomach. — (a) Ulceration from 
ulcer or cancer, if) Disease of the blood-vessels, such as 
miliary aneurysm, atheromatous or fatty degeneration, or 
varices of the veins. 

3. Congestion of the Gastric Mucous Membrane. — [a) Ac¬ 
tive congestion. This condition may occur with acute 
gastritis. Under this heading may be included vicarious 
menstruation by way of the stomach, (b) Passive conges¬ 
tion. This condition occurs with cirrhosis of the liver, 
thrombosis of the portal vein, or pressure on the vein by a 
tumor. It occurs secondarily with chronic diseases of the 
heart or of the lungs attended by general venous conges¬ 
tions. Congestion of the stomach often arises from splenic 
enlargement, being explained by the intimate relations 
between the vasa brevia and the splenic circulation. Con¬ 
gestion occasionally occurs during the expulsive efforts of 
parturition. 

4. Disorganized Blood-conditions. — (a) Haematemesis may 
occur with any of the severe infectious diseases, especially 
yellow-fever, small-pox, measles, scarlet fever, relapsing 
fever, malaria, and typhus fever. In these cases it is usually 
associated with other hemorrhages from mucous membranes 
and under the skin, (b) Toxic conditions, such as cholaemia 
and poisoning from phosphorus. ( c ) Hemorrhagic diseases. 
Among these diseases are to be mentioned scorbutus and 


HEMORRHAGE FROM THE STOMACH 


473 


purpura haemorrhagica. Under this heading may be in¬ 
serted haemophilia. ( d ) Profound anaemia, whether idio¬ 
pathic, malarial, leukaemic or pseudo-leukaemic, or due to 
Addison’s disease. 

5. Nervous Causes .—There are cases of haematemesis not 
infrequently occurring in hysterical subjects without assign¬ 
able cause. The disease is not uncommon with progressive 
paralysis of the insane and with epilepsy. 

6. Idiopathic Hemorrhage .—This condition was described 
by Flint as hemorrhage occurring, as it often does from the 
nose, without assignable cause, and not being due to any 
morbid condition. 

7. Melcena Neonatorum .—This is a severe and usually fatal 
hemorrhage occurring in infants within the first two weeks 
of life. It may occur in healthy children or in those with a 
family history of haemophilia, or it may occur in prema¬ 
turely born children from too early an interruption of the 
fetal circulation. In some cases it depends on gastric ulcer. 

8. The blood may not come primarily from the stomach, 
but may flow into it. In haemoptysis, epistaxis, or bleeding 
from the throat blood may be swallowed, to be vomited 
later. Blood may trickle down from the oesophagus from 
rupture of varicose veins in its wall, from ulceration, or 
from rupture into it of a neighboring aneurysm. The blood 
may enter the stomach from rupture into it of an aneurysm 
of the abdominal aorta or one of its branches, or ulceration 
may perforate the heart or the lungs, allowing of haemor¬ 
rhage in this way. Nursing babies may swallow blood 
from the mother’s breast, as from cracked and bleeding nip¬ 
ples. Hysterical patients often swallow blood from slaugh¬ 
ter-houses, and vomit it to obtain the sympathy of friends. 

The symptoms consist of hemorrhage and anaemia. In 
rare cases the patient may die before any blood has been 
vomited or passed with the stools. In all cases of profuse 


474 MANUAL OF THE PRACTICE OF MEDICINE. 

hemorrhage some blood, and in rarer cases all the blood, 
may be passed by the bowels, giving the stools a black, 
tarry appearance. Water added to such stools will develop 
a more characteristic blood color. The amount of blood 
lost may amount to three or four pounds in the course of a 
single day. Anaemic symptoms are marked in proportion 

to the amount of blood lost. 

Diagnosis.—Careful inspection usually leaves no doubt 
that it is blood that is vomited. Should doubt exist, re¬ 
course may be had to the microscope, the spectroscope, and 
the test for haem in-crystals. The diagnosis from haemop¬ 
tysis is to be based upon the points contained in the follow¬ 
ing table, compiled by Welch : 


Haemoptysis. 

1. Usually preceded by symptoms 
of pulmonary or cardiac disease. Bron¬ 
chial hemorrhage without evidence of 
preceding disease is not rare. 

2. The attack begins with a tickling 
sensation in the throat or behind the 
sternum. The blood is raised by cough¬ 
ing. Vomiting, if it occurs at all, fol¬ 
lows the act of coughing. 

3. The blood is bright red, fluid or 
but slightly coagulated, alkaline, frothy, 
and frequently mixed with muco-pus. 
If the blood has remained some time 
in the bronchi or in a cavity, it be¬ 
comes dark and coagulated. 

4. The attack is usually accompa¬ 
nied and followed by localized moist 
rales in the chest, and there may be 
other physical signs of pulmonary or 
cardiac disease. Bloody sputum con¬ 
tinues for some time, often for days, 
after the profuse hemorrhage ceases. 


Hcematemesis. 

1. Usually preceded by symptoms 
of gastric or hepatic disease, less fre¬ 
quently by symptoms of other diseases. 

2. The attack begins with a feeling 
of fulness in the stomach, followed by 
nausea. The blood is expelled by 
vomiting, to which cough, if it occurs, 
is secondary. 

3. The blood is dark, often black 
and grumous, sometimes acid, and usu¬ 
ally mingled with the food and other 
contents of the stomach. If the blood 
is vomited at once after its effusion, it 
is bright red and alkaline; or it may 
be alkaline if it is effused into an empty 
stomach. 

4. After the attack the physical ex¬ 
amination of the lungs is usually nega¬ 
tive, but there are generally symptoms 
and signs of gastric or hepatic disease. 
Black stools follow profuse hsematem- 
esis. 





NEUROSES OF THE STOMACH. 475 

The treatment of haematemesis is considered under Gas¬ 
tric Ulcer, page 462. 

NEUROSES OF THE STOMACH. 

Nervous Dyspepsia. 

Under this heading are included those cases of dyspepsia 
in which the stomach is apparently healthy and in which 
digestion is performed within the physiological time-limit. 

Etiology. —The condition is met with in those who are 
overworked, nervous, and worried, and in hysterical and 
neurasthenic patients. 

Symptoms .—Gastric symptoms resemble those of chronic 
gastritis in the main, but are less localized; vomiting rarely 
occurs, the symptoms are less dependent upon eating, and 
the tongue is less apt to be coated than in chronic gas¬ 
tritis. Chemical examination of the gastric juice allows 
of classification into three chief types : Nervous dyspepsia 
(1) with normal secretion, (2) with diminution of hydro¬ 
chloric acid, and (3) with the condition of hyperacidity or 
hypersecretion. The characteristic gastric symptoms of 
the last type are discussed under a separate heading. 

Intestinal symptoms consist of flatulence and irregularity 
in the action of the bowels. 

Nervous symptoms antedate the dyspepsia and are aggra¬ 
vated by it, a vicious circle being thus established. The 
general condition is one of neurasthenia of any grade of 
severity. Hypochondriasis is almost always present. 

The diagnosis of the nervous form of dyspepsia is to be 
made by the exclusion, so far as possible, of organic disease 
of the stomach and by the presence of a marked neuras¬ 
thenic element. It is often difficult to differentiate between 
chronic gastritis with resulting neurasthenia and a primary 
neurasthenia with the symptoms of nervous dyspepsia. In 


476 MANUAL OF THE PRACTICE OF MEDICINE. 

the majority of cases the diagnosis is rather a matter of 
professional instinct. 

The prognosis depends upon the curability of the under¬ 
lying neurasthenia. 

Treatment is to be directed to the general condition. 
Patients are apt to over-diet and to run themselves down. 
This should not be permitted, but a liberal, wholesome diet 
should be insisted upon. In obstinate cases with well- 
marked neurasthenic symptoms the Weir Mitchell rest- 
cure often yields brilliant and permanent results. 

Hypersecretion and Hyperacidity. 

Under these terms are included cases of gastric distress 
due to an excessive secretion or an increased acidity of the 
gastric secretions. Normally the gastric juice is secreted 
only when required for digestion, but in hypersecretion the 
process continues during fasting. Hypersecretion may be 
continuous or periodic, the latter form being usually asso¬ 
ciated with locomotor ataxia or with profound neurasthenia. 
Hyperacidity is more commonly observed, and is one of the 
complications of gastric ulcer. 

Symptoms.—Pain, which is of a gnawing, burning char¬ 
acter, is referred to the epigastrium or the heart, or it may 
be substernal. It is often spoken of as “ heartburn.” There 
are eructations of an acid fluid setting the teeth “ on edge,” 
and vomiting of a clear acid fluid may occur. Pain and acid 
eructations may occur with acid fermentation of the con¬ 
tents of the stomach, but the symptoms occur soon after 
eating, are not relieved by eating, and the eructated fluid 
contains fermenting particles of food; whereas the symptoms 
of hypersecretion or of hyperacidity occur when the stomach 
is empty, are relieved by eating, and the eructations consist 
of fluid alone. Digestion is usually retarded, especially for 
the starches. 


NEUROSES OF THE STOMACH. 


477 


The diagnosis of hypersecretion may be made by finding 
an acid secretion in the stomach during fasting hours. 
Hyperacidity is determined by the quantitative analysis of 
the gastric juice, obtained through a stomach-tube one 
hour after an Ewald test-breakfast consisting of a Vienna 
roll and a cup of weak tea without milk or sugar. 

Treatment.—Neurasthenic conditions demand appropri¬ 
ate treatment. Alkalies in large doses (sodium bicarbonate, 
3 j—ij) should be given two or three hours after meals, and 
may be combined with cannabis indica (gr. Herri ng’s Eng¬ 
lish extract). This combination not only relieves the pain 
and distress, but seems to have a decided curative effect. 
In obstinate cases a strictly meat diet may be enforced, or 
the stomach may be washed out with a weak alkaline solu¬ 
tion every day before the principal meal. 

Gastralgia ; Gastrodynia. 

Neuralgic pain in the stomach may occur as a symptom of 
organic disease, as ulcer or cancer, or in the form of the 
“ gastric crises ” of locomotor ataxia. Aside from these 
cases, gastralgia may occur as a functional neurosis, inde¬ 
pendent of organic disease, and to this form the term “ gas¬ 
tralgia” should properly be confined. 

Etiology. —Most patients are neurasthenic, hysterical 
women, usually those at the change of life, but young 
women and men may also be affected. The attack seems to 
be favored by a gouty tendency, malarial poisoning, hys¬ 
teria, and hyperacidity or hypersecretion. Gastralgia is one 
of the regular symptoms of chronic poisoning by lead. 
The attacks may be induced by excessive chewing of to¬ 
bacco or by over-indulgence in tea. 

Symptoms. —The disease appears in attacks of gastric 
pain, of a burning, tearing, or boring character, usually 
referred to the epigastrium, and occasionally radiating to the 


478 MANUAL OF THE PRACTICE OF MEDICINE. 

back and around the waist. Light pressure is grateful, but 
tenderness is usually elicited by firm pressure. Vomiting 
is rare. Relief is frequently afforded by eating. During 
the attack the abdomen is usually retracted, and the patient 
assumes a generally flexed position. The attacks, which 
last from a few minutes to several hours, may be repeated 
at irregular intervals, or they may occur with such peri¬ 
odicity as to suggest a malarial influence. They may recur 
at night, and they are usually independent of eating, al¬ 
though in some cases pain may arise from dietetic causes. 
The symptoms of gastralgia are usually associated with 
those of a neurasthenic or hysterical nature, giving a de¬ 
cidedly neurotic stamp to the majority of cases. 

The diagnosis is to be made by the exclusion of organic 
lesions and by the general view of the case, showing admix¬ 
ture of neuralgic and neurasthenic symptoms. The diag¬ 
nosis is often made with great difficulty. 

The prognosis depends upon the curability of the under¬ 
lying cause. 

Treatment.—For the attack itself, hot applications or a 
mustard paste may be applied to the epigastrium. Carmin¬ 
atives are often of service—Hoffmann’s anodyne, spirits of 
chloroform, or valerian. Morphine is not to be used, on 
account of the possibility of a habit being formed; while 
cocaine is not recommended, because of its extreme depres¬ 
sant effect. Relief is frequently afforded during an attack 
by copious draughts of hot water. To prevent recurrences 
the underlying cause should be detected and removed. 
Neurasthenic conditions require appropriate treatment. 
Arsenic in free doses, but not to the point of tolerance, fre¬ 
quently acts as a specific. The combination of valerianate 
of zinc (gr. iij) with small doses (gr. |) of nitrate of silver is 
often useful. Hyperacidity and hypersecretion, if present, 
require their special treatment. 


NEUROSES OF THE STOMACH 


4/9 


Nervous Vomiting. 

Nervous vomiting does not arise from organic disease, 
but is a pure motor neurosis depending upon cerebral or 
reflex irritation. 

Etiology. —Nervous vomiting may accompany lesions of 
the brain, the cord, or the meninges, hysteria, neurasthenia, 
or migraine. It may be due to reflex irritation from lesions 
of the abdominal or pelvic organs, and it occurs with sea¬ 
sickness and pregnancy. In neurasthenic males nervous 
vomiting may be due to irritation of the genito-urinary 
organs. The gastric crises of locomotor ataxia are described 
elsewhere. The “ periodical vomiting ” of Leyden is asso¬ 
ciated with gastric pain ; it occurs in anaemic and nervous 
patients. 

The symptoms of nervous vomiting differ from those of 
ordinary vomiting in that nausea and retching are seldom 
observed. It is rather a regurgitation than a vomiting. 
Food is usually ejected after meals, but the vomiting, which 
may occur at irregular intervals, is so little dependent upon 
dietetic errors that the name “ causeless vomiting ” is often 
applied to these cases. In hysterical cases, although all 
food may apparently be vomited, the general nutrition may 
remain good. 

Treatment is to be directed to the underlying cause. 
Change of climate is often of great service, especially in 
cases of the primary periodic vomiting of Leyden. 

Peristaltic Unrest. 

Peristalsis of the stomach is increased, with the produc¬ 
tion of loud splashing sounds often heard at a considerable 
distance. This condition is not uncommon in neurasthenic 
subjects; it is usually increased by emotions. 


480 MANUAL OF THE PRACTICE OF MEDICINE. 

Rumination ; Merycismus. 

Hysterical and feeble-minded patients may regurgitate 
the food and chew the cud like ruminating animals. The 
habit is frequently hard to cure, but it seems to exert no 
evil effect upon the general health. 


3. DISEASES OF THE INTESTINES. 

MORNING DIARRHOEA. 

The etiology and pathology of morning diarrhoea are 
unknown. It is probable that the disease is functional and 
not inflammatory. 

The symptoms consist of diarrhoea, usually limited to 
the early morning hours. There may be but one passage, 
or the diarrhoea may continue throughout the forenoon. 
The passages are usually painless and are accompanied by 
the passage of flatus. The diarrhoea may be varied by 
periods during which the bowels are normal or consti¬ 
pated. Mental worry is usually associated with the dis¬ 
ease, and exhaustion may occur should the diarrhoea be 
excessive. In protracted cases the diarrhoea begins at an 
earlier hour of the morning, so that patients may be awak¬ 
ened at four or five o’clock in the morning with pain and 
an urgent desire for stool. In long-continued cases there 
may be developed a sense of impending movement of the 
bowels whenever any food is taken into the stomach. 

Treatment. —A change of climate is frequently followed 
by a most brilliant result, which in the majority of cases is 
permanent. The general health should be built up; various 
modifications of diet should be tried, such as diets from 
which the starches and sugars are excluded, or a diet of 
meat alone. The treatment by drugs is not satisfactory, 



ACUTE CATARRHAL ENTERITIS. 48 I 

but salol, naphthaline, and the subgallate of bismuth may 
be used. Delafield finds his best results to have followed 
castor oil in doses of from 5 to 10 drops. 

ACUTE CATARRHAL ENTERITIS. 

Synonyms.—Acute ileo-colitis; Acute entero-colitis; 
Acute intestinal catarrh ,* Acute diarrhoea. 

While certain portions of the small intestine may be in¬ 
flamed more than others, it is not usually possible during 
life to say which portion is especially involved. In the 
great majority of cases the small intestine throughout its 
length is affected, together with the upper portion of the 
laige intestine, and to this condition the names of “enter¬ 
itis ” and “ entero-colitis ” are applied. 

Duodenitis causing catarrhal jaundice will be considered 
under the latter heading-. 

Etiology. The causes may be primary or secondary. 

Pi unary Causes. 1. Error in food, either in quantity or 
in quality. The commonest cause is the ingestion of unripe 
fiuit 01 of food or milk in which decomposition-changes 
have taken place before its ingestion. Individual peculiari¬ 
ties play a considerable part in the causation of the disease, 
for what is food for one may be poison for another. 

2. Impuiities in drinking-water often cause epidemics of 
enteritis. Strangers are more susceptible to such impurities 
than are those who are accustomed to the water. 

3. Toxic causes, such as irritant food or drugs, either 
alkaline, acid, or corrosive. 

4. A sudden fall in temperature or the chilling of the 
surface after excessive perspiration may induce an attack. 

5. Changes in the intestinal secretions may theoretically 
give rise to conditions leading to catarrh, but of these 
changes we know practically but little. 

Secondary Causes .— 1. Enteritis is often secondary to any 

n 





482 MANUAL OF THE PRACTICE OF MEDICINE. 

gastric cause allowing fermenting or undigested food to pass 
into the intestine. 

2. Peritonitis or any organic disease of the intestine, such 
as ulcer, hernia, or cancer. 

3. Enteritis is favored by any chronic congestion of the 
intestinal blood-vessels from chronic heart or lung disease, 
or by any cause producing obstruction in the portal circu¬ 
lation. 

4. Enteritis often occurs in the course of acute infectious 
disease; it may attend chronic cachectic conditions, such as 
those occurring with cancer, tuberculosis, Bright’s disease, 
or anaemia. 

Pathology.—The mucous membrane is red, swollen, con¬ 
gested, and covered with mucus. These pathological ap¬ 
pearances often disappear after death, leaving the mucosa 
pale and sodden. The solitary and agminated glands are 
swollen and prominent, especially in children. Follicular 
and catarrhal ulceration may occur. 

Symptoms.—There is pain of a colicky character, which 
may be diffused or may be localized at the umbilicus. It is 
usually worse before an evacuation, and is generally relieved 
by firm pressure. A tendency to straining indicates that the 
lower portion of the colon is involved. Tympanites and 
gurgling noises or borborygmi usually accompany the attack, 
being due to the presence of fluid and gas within the intes¬ 
tine and to increased peristalsis. If the inflammation be con¬ 
fined to the small intestine, there need be no diarrhoea. If the 
colon be involved, there is a loose fecal diarrhoea, the thin, 
gruel-like stools often containing portions of undigested food 
(lienteric diarrhoea) and flakes of brownish mucus. The color 
of the stools varies from dark brown to yellow, or even to 
gray, according to the amount of bile with which they are 
mixed. The number of evacuations varies from three or four 
up to twenty in the course of the day. There is usually loss 


CHRONIC CATARRHAL ENTERITIS. 


483 

of appetite, with occasionally nausea or vomiting 1 . Fever 

may be absent, or there may be a rise of temperature of a 
few degrees. 

The prognosis is perfectly good, the attack lasting from 
five days to a week and terminating in recovery. Relapses 
are frequent from repetitions of the original exciting cause. 

Treatment.—In mild cases rest and a restricted diet suf¬ 
fice. The dietetic rules to be observed in chronic gastritis 
aie applicable to these cases. In more severe cases a milk 
diet during the acute attack may be indicated. The patient 
should be kept warm, and a flannel band over the abdomen 
is of service, particularly in children. A cathartic is usually 
indicated at the onset, despite the existence of diarrhoea. 
The best drug for this purpose is castor oil or calomel. It 
is not wise to check diarrhoea for forty-eight hours. After 
this time asti ingents may be given, combined with opium 
in small doses. Bismuth subnitrate in gr. xx—xxx doses 
every two hours is usually efficient. Pain may be controlled 
by hot applications to the abdomen, by small doses of opium, 
or by spirits of chloroform in £ss doses. 

CHRONIC CATARRHAL ENTERITIS. 

Etiology and Synonyms.—The most frequent cause of 
chronic catarrhal enteritis is the continuance of improper 
food and hygiene. It may follow repeated acute attacks; 
it follows chronic congestion of the portal circulation, 
chronic lung and heart diseases, and diseases of the liver, 
such as cirrhosis or pressure on the portal vein. It may 
occur with chronic lesion of the intestine, such as cancer or 
tubercular ulceration. Cachectic and debilitated conditions 
predispose to the disease, and it seems to be more common 
in those with a gouty tendency. Synonyms: Chronic intes¬ 
tinal catarrh; Chronic diarrhoea; Chronic catarrhal entero¬ 
colitis. 


484 MANUAL OF THE PRACTICE OF MEDICINE. 

Pathology.— The lesion is a chronic catarrhal inflamma¬ 
tion of the small, and usually of the large, intestine. The 
mucous membrane is generally congested and covered with 
mucus, and the wall of the intestine is thickened by hyper¬ 
trophy of all its layers. In other cases the wall of the in¬ 
testine is thinned, the glandular elements undergo atrophy, 
and the mucous membrane is grayish or lead-colored. The 
lymph follicles are swollen and pigmented. Pigmentation 
of the villi also occurs. Catarrhal or follicular ulceration 
is seen in severe cases, the latter form being especially well 
marked in the lymph-follicles of the descending colon and 
the sigmoid flexure. The close approximation of these con¬ 
ical ulcers often gives to the colon a sieve-like or honey¬ 
combed appearance. These ulcers may perforate or be the 
seat of hemorrhage. 

The symptoms of chronic catarrhal enteritis resemble 
those of acute entero-colitis, but are more protracted. As 
the large intestine is almost regularly involved, diarrhoea is 
a prominent symptom in most cases. In othei patients 
diarrhoea alternates with periods of constipation. The stools 
usually are thin and fecal, containing undigested food mixed 
with mucus. If mucus be evenly admixed with the stool, 
its source is probably the small intestine 5 if it coat the stool, 
it comes from the large intestine. The patient frequently 
passes lumps or strings of glairy mucus, which may com¬ 
prise the entire stool. Blood or pus may be present in the 
dejecta, the presence of the latter being a sure indication of 
the existence of ulceration. The number of stools varies 
from one to eight in the course of the day. In some cases 
the diarrhoea occurs in the early morning hours ; in other 
cases it is induced by eating. 

Pain to some degree is usually present. It may be dif¬ 
fused, or localized at the umbilicus and of a colicky cha¬ 
racter. It is most common in from one to three hours after 


CHRONIC CATARRHAL ENTERITIS. 485 

eating. In other cases there is only a sense of oppression 
and fulness. Borborygmi and flatulence accompany the 
disease, and there may be symptoms of an associated gas¬ 
tritis or of functional disturbance of the liver. In aggra¬ 
vated cases the general health fails, the patient becoming 
thin and weak, and the emaciation and prostration may be 
extreme. Hypochondriasis or melancholia may occur. 

The prognosis for perfect recovery is usually bad, although 
much may be done to relieve the patient. There are usually 
periods of temporary improvement, even if the case be not 
treated. The disease may be fatal in debilitated and aged 
patients and in children. The rare accident of perforation 
should not be forgotten. 

Treatment should be carried out faithfully and patiently. 
The diet should be regulated to suit the peculiar needs of 
each case. As a rule, starches, sugars, and fats are objec¬ 
tionable. In aggravated cases recourse may be had to a 
meat or an exclusive milk diet. The bowels should be 
regulated. If constipation exists, cascara, podophyllin, aloin, 
or compound extract of colocynth may be used. A good 
combination to be recommended is the following : 


1 ^. Strychninse sulphatis, gr. JL . 

Resin, podophylli, gr. A ; 

Ext. belladonnae, gr. i • 

Pulv. ipecac., gr. I —M. 

Ft. pil. No. j. 


Sig. Such a pill after each meal. 

Massage or faradization of the abdomen may be employed. 
If diarrhoea is present, astringents with intestinal disinfect¬ 
ants are indicated. Among these may be mentioned sub¬ 
nitrate of bismuth, 3ss-j; subgallate of bismuth, gr. x-xx; 
naphthaline, gr. x-xv; salicylate of bismuth, gr. x-xx; or 
salol, gr. v-x,—these doses being repeated three or four 


486 MANUAL OF THE PRACTICE OF MEDICINE . 

times in the day. Opium should not be given as a routine 
treatment. If the diarrhoea depend upon ulceration of the 
colon, large colon injections should be used. The hips 
being elevated, the injection should be allowed to flow in 
gradually from a fountain bag; in this way from two to 
four pints of injection are to be introduced, and it may 
be retained for some time. Simple water containing 3j of 
soda or borax or salt to the pint may be used ; the addi¬ 
tion of an astringent is seldom, if ever, necessary. The 
stools should be examined to see what classes of food 
are undigested, and suitable dietetic regulations should be 
enforced. Meat, as a rule, is poorly borne. In all cases 
care should be taken to build up the general health and to 
avoid exposure to cold. A flannel abdominal bandage should 
be worn constantly. In some cases the best results are ob¬ 
tained by sending the patient to spend the winters in a warm, 
dry climate. 


PHLEGMONOUS ENTERITIS. 

This affection is exceedingly rare as a primary disease, 
but it may occur in connection with ulceration of the intes¬ 
tine, strangulated hernia, and intussusception. The puru¬ 
lent infiltration may be localized or diffused. 

Symptoms.—The primary cases run a peracute course, 
with pain, tympanites, constipation, and fever, and terminate 
by septic peritonitis. These cases appear to be due to in¬ 
fection by the bacterium coli commune. The symptoms 
of the secondary cases may be obscured by those of the 
primary disease, so that the diagnosis is seldom made. 

Prognosis.—The disease is rapidly fatal. 

PSEUDO-MEMBRANOUS ENTERITIS. 

Etiology and Synonyms.—Pseudo-membranous enteritis 
occurs (a) as a secondary process in acute infectious dis- 


MUCOUS COLITIS. 


48; 

eases, especially typhoid fever, scarlet fever, and cholera; 
iP) as a complication of dysentery or of intestinal obstruc¬ 
tion; (o) in conditions of advanced cachexia; (d) as the 
result of poisoning by mercury, lead, and arsenic, and in 

uraemic conditions. Synonyms: Diphtheritic or Croupous 
enteritis. 

Pathology.—The pseudo-membranous inflammation is 
usually more marked in the colon, but, especially in the 
mercurial and uraemic forms, the small intestine may also 
be involved. Necrosis, ulcerations, perforation, or hemor¬ 
rhage may result, or cicatricial obstruction may ultimately 
develop. 

The symptoms are latent in many cases secondary to 
acute infectious diseases and to cachectic states. In other 
cases, especially in the mercurial form, the symptoms of a 
violent entero-colitis are developed. Stools consisting of a 
thin, purulent liquid containing blood and shreds of the 
pseudo-membrane are fairly characteristic of this affection. 
Hemorrhage and perforative peritonitis are common com¬ 
plications. 

This disease should not be confounded with membranous 
or mucous colitis—an entirely distinct disease. 

The treatment is that of a severe acute entero-colitis. 
Opium should be given to limit peristalsis and to diminish 
the danger of perforation or hemorrhage. 

MUCOUS COLITIS. 

Etiology.—This affection regularly occurs in neuras¬ 
thenic and hysterical patients. Over 80 per cent, of cases 
occur in women, especially in those who have suffered from 
uterine disease or from dyspepsia. It is essentially a dis¬ 
ease of adult life, but a few cases occur in children. Syn¬ 
onyms: Mucous colic; Membranous colitis; Mucous diar¬ 
rhoea. 


488 MANUAL OF THE PRACTICE OF MEDICINE. 

Pathology.—There are no evidences of inflammation, 
but the disease seems to be due to a derangement of the 
mucous follicles of the colon. The exact nature of the dis¬ 
ease is, however, unknown. 

The symptoms appear in attacks characterized by severe 
colicky pain with tenderness over the abdomen, followed by 
the passage of mucus in flakes or strings or as casts of the 
lining of the bowel. Mucus is not, however, passed with 
every paroxysm. The attacks may last for several days or 
weeks; they may be produced by errors in diet or by 
mental worry, and they often occur in the early morning 
hours. The strings of mucus frighten the patients into the 
belief that the “ lining of the bowel is ulcerated and is 
coming away,” so that they become hysterical and hypo¬ 
chondriacal. Between the attacks the symptoms of neur¬ 
asthenia are regularly present; they become more marked 
before and during the paroxysms. 

The course of the disease is often chronic, the attacks 
recurring at intervals for years. 

The diagnosis is easily made if the mucus be not mis¬ 
taken for other substances, such as intestinal parasites and 
shreds of undigested food. The long continuance of the 
disease, the absence of fever, and the exciting role played 
by neurasthenia and the emotions serve to distinguish the 
disease from diseases of an organic basis. 

The prognosis is good if the neurasthenia can be relieved. 

Treatment consists primarily in the cure of the neuras¬ 
thenia. The Weir Mitchell rest-cure should be tried in 
obstinate cases, while in all instances the nutrition should 
be improved in every way. Forced feeding, especially by 
cream and cod-liver oil, is often beneficial, and it can be said 
that the prognosis is good if the patient can be made to gain 
in weight. 

Morphine is not to be used during a paroxysm, for fear 


DIARRHCEAL DISEASES Of CHILDREN. 489 

of the habit being formed. High enemata of warm salt-solu¬ 
tion (3j : Oj) may be given every day to cleanse the colon and 
to bring away the mucus. At least two quarts of the solution 
should be allowed to enter the bowel slowly, the patient 
lying on the left side with the hips elevated. Astringent and 
irritating enemata should not be used. Dietetic errors and 
digestive disturbances should receive appropriate treatment. 

DIARRHCEAL DISEASES OF CHILDREN. 

General Etiology.—Diarrhoeal diseases occur with espe¬ 
cial frequency among artificially fed children between the 
ages of six and eighteen months, and tenement-house and 
asylum children are more apt to be attacked. Owing to 
the small size of the child’s stomach and to the deficiency 
in the saliva and in the proper acidity of the gastric secre¬ 
tions, dietetic errors result in graver consequences than in 
adults. The food may be given too freely or at irregular 
intervals, or the child may partake of food suitable only 
for adults, and the result of these dietetic errors is intensi¬ 
fied by teething and by hot weather. Decomposed milk 
teeming with bacteria is perhaps the most common cause 
of infantile diarrhoea. The relation of bacteria to the diar¬ 
rhoeal affections of children has received careful attention. 
The healthy stools of children contain a number of micro¬ 
organisms, the most important of which are the bacterium 
coli commune and the bacterium lactis aerogenes, the latter 
being present only after a milk diet. These two bacteria 
are alone constantly present. In infantile diarrhoea there 
appear, in addition to the above-mentioned bacteria, a great 
number of micro-organisms, as many as forty varieties hav¬ 
ing been described. Acknowledging that these diarrhoeal 
diseases have a bacterial origin, no one germ can be re¬ 
garded as the specific cause, but a large number of differ¬ 
ent kinds are concerned. 


490 MANUAL OF THE PRACTICE OF MEDICINE. 

Classification.—Three distinct forms of acute infantile 
diarrhoea are to be described : I. Acute dyspeptic diar¬ 
rhoea; 2. Acute entero-colitis; 3. Cholera infantum. 

Acute Dyspeptic Diarrhcea. 

Acute dyspeptic diarrhoea, which is caused by the irrita¬ 
tion of undigested or tainted food, is due to increased in¬ 
testinal peristalsis. 

Symptoms.—The stools, which are rarely more frequent 
than five or six in the twenty-four hours, consist of lumpy 
masses of undigested milk or food. They are not watery, 
and they contain no mucus. Their color is yellow, mixed 
with green, usually changing to green on exposure to the 
air. There may be vomiting of food and of mucus. Col¬ 
icky pain usually precedes each stool, and the abdomen 
may be distended with gas. Convulsions or carpopedal 
spasms may occur in nervous children. In mild cases 
there may be no fever, but in the severer forms and in the 
case of children naturally feverish the temperature may 
reach 104° or even 105 0 F. The attack usually terminates 
when the intestine has been relieved of its irritating con¬ 
tents; it may, however, prove fatal in sickly children. In 
hot weather and in neglected cases the disease may develop 
into entero-colitis. 

Treatment.—The bowels should be moved freely by 
castor oil or calomel, even if the condition of diarrhcea 
persist. Food should be withheld for a time until the 
stomach is settled, but cracked ice or cool water may be 
given. After the bowels have been moved by medication, 
bismuth and chalk mixture may be given. 

Acute Entero-colitis. 

Acute entero-colitis is the ordinary form of summer diar¬ 
rhoea in children. It is the dreaded scourge of tenement- 


D/ARRHCEAL DISEASES OF CHILDREN. 491 

house children in their second summer, and it often appears 
as a sequel to the specific diseases of children. The ileum 
and the colon are the seat of a catarrhal inflammation, the 
follicles being especially involved, and frequently ulcerated, 
so that the name “ follicular enteritis ” or “ follicular dysen¬ 
tery ” is sometimes applied to these cases. In severe cases 
the inflammation may be of the pseudo-membranous 
variety. 

Symptoms.—The disease usually follows acute dyspeptic 
diarrhoea. The general condition of the child becomes 
worse. The temperature rises and remains constantly high, 
although extreme hyperpyrexia is but seldom observed. The 
stools become small in size, vary between twelve and thirty 
in the twenty-four hours, contain a large quantity of mucus 
frequently mixed with blood, and are acid and offensive. They 
may be passed painlessly, or with straining and tenesmus 
if the rectum be involved, or colicky pain may precede the 
movement Flatus is usually passed in considerable amount, 
and the abdomen is distended, hard, and usually tender along 
the line of the colon. Vomiting may occur, but it is rarely 
a marked feature of the disease. The attack may last for 
several weeks and may terminate by recovery or by death 
from inanition and exhaustion, or the affection may become 
protracted. In this form the acute symptoms disappear, 
but the diarrhoea continues and nutrition does not improve. 
From this subacute enteritis the child may convalesce in 
from six to eight weeks, or the disease may become 
chronic. 

In some cases of entero-colitis the follicular glands of the 
colon are extensively involved, leading to the symptoms 
frequently spoken of as the “acute dysentery of children.” 
The onset is sudden, with fever, convulsions in the severer 
forms, and frequent small passages almost entirely com¬ 
posed of mucus and blood, and not containing feces. There 


492 MANUAL OF THE PRACTICE OF MEDICINE . 

are incessant abdominal pain and rectal tenesmus. In mild 
cases the bowels can be opened within two or three days 
by castor oil, and recovery rapidly ensues; but if the 
bowels cannot thus be moved, the case is apt to continue 
from three to six weeks, or even to become chronic. 

There is a rare form of entero-colitis, of great severity, 
characterized by high fever, dysenteric symptoms, convul¬ 
sions, stupor, and collapse. 

Treatment. —Attention to the proper feeding of the child 
is of the utmost importance. The diet should consist of 
sterilized or peptonized milk or of albumin-water. Cream 
and water are often better borne than milk. After the irri- 
tatino- cause has been removed, bismuth and chalk mixture 

o 

should be given, to which any of the intestinal antiseptics 
may be added. Of these, bismuth salicylate, bismuth sub- 
gallate, and salol are perhaps the most reliable. Large 
enemata of salt-solution (gj: Oj) should be used to flush out 
the colon ; they are of the greatest service. The addition 
of astringents to these enemata is not to be recommended. 
Should dysenteric symptoms occur, the bowels should be 
opened with castor oil, and this medication should be 
repeated every other day. Medicated enemata may in these 
cases be used, as in the dysentery of adults. 

Cholera Infantum. 

The term “ cholera infantum ” has been applied loosely to 
any diarrhoea of childhood with vomiting and prostration, 
but it should be limited to a special group of symptoms 
resembling cholera morbus of the adult. The term being 
limited in this way, cholera infantum is rather a rare disease, 
occurring in only 2 or 3 per cent, of the summer diarrhoeas 
of children. Cholera infantum is essentially a bacterial dis¬ 
ease, the symptoms being due to poisoning by the ptomaines 
generated by the action of the bacteria upon milk or other 


DIARRHCEAL DISEASES OF CHILDREN. 493 

intestinal contents, although no one organism can be de¬ 
scribed as a specific cause. 

Pathology.—There is an acute gastro-enteritis, although 
the appearances of inflammation may disappear after death, 
leaving the mucous membranes pale and sodden. The 
lymph-glands of the intestine may be swollen, and in rare 
instances may soften and break down to form follicular 
ulcers. Various micro-organisms may be found in the mes¬ 
enteric glands and in the lymphatic vessels of the intestinal 
wall. 

The symptoms of cholera infantum may begin abruptly, 
or there may be a preliminary diarrhoea for several days. 
The first regular symptom is purging. The stools, at first 
acid and fecal, later become alkaline, serous, and either 
colorless, brownish, or of the “ rice-water ” appearance. 
The passages are abundant, often are expelled with force, 
and in some cases amount to a constant discharge. The 
purging is supposed to result from paresis of the blood-ves¬ 
sels of the intestinal wall from the toxic action of the pto¬ 
maines, resulting in the abundant transudation of serum. 
There is, as a rule, neither abdominal pain nor tenderness, 
although in some cases colicky pain may precede the purg¬ 
ing in the earlier stages of the disease. Vomiting is not as 
constant as purging, but it may be violent and incessant, so 
that no food can be retained. The vomited matters consist 
first of food; later they are of a brownish or bile-stained 
serum, and may be like rice-water. The skin is cool and 
clammy, but the rectal temperature shows an increase to 
103°, 105°, or even 107° F., there being no disease of in¬ 
fancy regularly attended by so high a temperature. The 
pulse is rapid and thready. The skin may be firm and 
hard—a condition to which the names “ sclerema ” and 
“ frozen skin” have been applied. The appearance of the 
child is rapidly altered; the face is thin, drawn, and of an 


494 MANUAL OF THE PRACTICE OF MEDICINE . 

ashy paleness, the eyes are sunken, the fontanelle is de¬ 
pressed, and the loss of weight is evident. The urine 
becomes diminished or even suppressed, and uraemic symp¬ 
toms may develop. 

Course of the Disease.— I. A considerable number of 
the children die in from one to three days, from exhaustion, 
collapse, or with cerebral symptoms. These “ hydrocepha- 
loid ” symptoms, or “ pseudo-hydrocephalus,” consist of 
drowsiness merging into coma, muscular twitchings or con¬ 
vulsions, retraction of the head, and subnormal temperature 
or hyperpyrexia; the respirations become shallow and ir¬ 
regular, and may be of the Cheyne-Stokes variety. The 
pulse becomes irregular and flickering. The vomiting and 
purging usually cease for some hours preceding the fatal 
termination. 

2. Other patients begin to improve in from twenty-four 
to thirty-six hours, and the improvement is either rapid and 
complete or is complicated by a recurrence of the former 
symptoms. Chronic furunculosis may appear as a sequel. 

3. In some children improvement progresses only to a 
certain point, but the child still continues sick, with vomiting, 
diarrhoea, and prostration. In this condition the child may 
remain for weeks and then slowly recover; or the symptoms 
may continue, prostration and emaciation may become more 
and more marked, and the child may ultimately die from 
marasmus. 

The prognosis is always serious, especially in bottle-fed 
babies and in asylum and tenement-house children. A 
guarded prognosis must always be given, however mild the 
case may appear at the onset. 

Treatment.—The most important indication for treat¬ 
ment is the reduction of the hyperpyrexia. This should 
be accomplished by baths of 90° F. gradually reduced to 
8o° F. by the addition of cool water. Irrigation of the 


DIARRHCEAL DISEASES OR CHILDREN. 


495 


stomach and the colon is indicated in every case, to remove 
toxic products and to supply water to the tissues. For the 
purging, opium is almost indispensable, but the drug should 
be given to children with extreme caution, as they are pecu¬ 
liarly sensitive to its action. Morphine gr. yj-g- is a fairly 
large dose for a child of one year. As a practical rule, 
opium should not be given to babies under six months of 
age unless it be absolutely necessary to do so. 

Intestinal antiseptics should be given if they do not add 
to the vomiting. Of these, bismuth salicylate (gr. v q. 2 h.) 
is perhaps the most useful. Small doses of mercurial prep¬ 
arations often are of service in controlling the vomiting. 
Calomel (gr. mercury with chalk (gr. or bichloride 
of mercury (gr. may be given in these doses every two 
or three hours without danger of salivation. Stimulants 
may be given if indicated, and, should collapse appear, 
subcutaneous injections of a I per cent, saline solution 
(sterilized) may be given as in Asiatic cholera. Iced drinks 
may be given even if they are not retained. If the case be 
protracted, it is of the utmost importance to move the child 
to the country, where the air is cool and fresh. These little 
patients stand travel well, and the improvement is often 
striking within a few hours after the change has been made. 
The dietetic rules are those applicable to acute entero-colitis. 

Cholera infantum in meat-fed children presents certain 
peculiarities by which it differs from cholera infantum of 
milk-fed babies. The stools are not as watery, as frequent, 
nor as profuse as in the ordinary cases, but are grayish or 
yellowish-green and highly offensive. Tympanites is a con¬ 
stant symptom, but vomiting is more frequently absent. The 
general symptoms are those of sepsis, and death usually re¬ 
sults in from forty-eight to seventy-two hours. Mild cases 
may recover. 




496 MANUAL OF THE PRACTICE OF MEDICINE . 


CHOLERA MORBUS. 

Etiology and Synonym.—Cholera morbus is most com¬ 
mon in young adults and in the summer months. The 
attack may be induced by improper or partially decayed 
food, by unripe fruit, or by impure drinking-water. At 
times the disease assumes such epidemic proportions that 
it seems as though some specific micro-organism must act 
as the exciting cause. Synonym : Cholera nostra. 

Pathology.—The lesion consists of a catarrhal inflam¬ 
mation of the stomach and of the large and small intes¬ 
tines. The submucosa is infiltrated to some extent by 
fibrin, serum, and round cells, and the intestinal glands are 
swollen. It is impossible to differentiate cholera morbus 
from Asiatic cholera except by post-mortem examination, 
the comma bacillus being found in the latter disease. 

Symptoms.—The attack is usually sudden, although it 
may be preceded by oppression and by vague abdominal 
distress. The patient is usually attacked during the night 
or the early morning. There are nausea and faintness with 
violent and incessant vomiting, the ejected matter consist¬ 
ing at first of food and later of fluid, either colorless or 
tinged with bile. Following or coincident with the vomit¬ 
ing is severe purging, d he stools at first are feculent, but 
later become watery and odorless ; they consist of serum 
with flakes of desquamated epithelium, giving to the stools 
the so-called “rice-water” appearance. The color of the 
passages is usually greenish or yellowish, and the fluid is 
sufficiently acrid to irritate and excoriate the anal parts. 
Cramps in the abdomen cause tearing, lacerating pain, usu¬ 
ally referred to the umbilicus, but in some cases the purging 
is painless. There may be violent muscular cramps, espe¬ 
cially in the calves of the legs, due to the dryness of the tis¬ 
sues. Prostration appears early in the attack. The face is 


D YSENTER Y. 


49 / 


drawn and anxious; the pulse is rapid and thready; the 
skin is cold and clammy, but the internal temperature 
reaches ioi° or 102° F., or even higher than this. 

The duration of the attack varies from a few hours to 
several days. 

The prognosis is good. The disease may, however, be 
fatal in debilitated subjects, so that the whole mortality is 
between 2 and 3 per cent. 

The diagnosis from Asiatic cholera cannot be made with 
certainty without bacterial examination of the stools. 

Treatment is entirely symptomatic. As drugs cannot 
be retained when given by the mouth or the rectum, hypo¬ 
dermic medication alone is to be relied upon. Morphine 
in gr. doses should be given, and repeated if necessary, 
to check the pain, vomiting, and purging. Hot poultices 
applied to the abdomen afford relief. For the attendant 
thirst cracked ice may be allowed if it does not increase 
the vomiting. It is well to give no food by the mouth 
until the attack is well over, and then food may be allowed 
in small quantities at first and at frequent intervals. 

DYSENTERY. 

Etiology. —Dysentery is essentially a disease of the 
tropics, where “ it destroys more lives than cholera, and it 
has been more fatal to armies than powder and shot ” (Osier). 
Under imperfect hygiene sporadic and endemic cases occur 
in Northern cities,, and even epidemics may occur, but with 
improved sanitation the disease is much less common than 
formerly. The exciting cause has been supposed to be 
drinking-water contaminated by animal matter, while in the 
tropics one form of dysentery appears to be due to infection 
by the amoeba coli. Dysentery attacks patients of all ages, 
and there is no racial exemption. The majority of cases 
occur in the late summer and early fall months. 

32 


498 MANUAL OF THE PRACTICE OF MEDICINE. 

Varieties. —The following varieties are to be described: 
1. Acute catarrhal dysentery; 2. Amoebic or tropical dys¬ 
entery ; 3. Acute croupous dysentery; 4. Chronic dysentery. 

Acute Catarrhal Dysentery. 

This orm is the one usually seen in temperate climates. 

Pathology. —The inflammation is limited to the large 
intestine, especially to the sigmoid flexure and the rectum, 
but the lower portion of the ileum may also be involved. 
The mucous membrane is swollen, congested, and covered 
with tenacious blood-stained mucus. The solitary glands 
are prominently enlarged, and in severe cases may ulcerate. 
In the crravest form of the disease the follicular ulceration 

o 

may deepen and spread, more extensive ulcerations being 
formed. In children the inflammation and ulceration of the 
follicles are more marked than in adults, so that the disease 
is often spoken of as “ acute follicular dysentery.” 

The symptoms differ according to whether the rectum 
or the upper colon be involved. 

I. If the rectum be involved, as it is in the vast majority 
of cases, there may be a preliminary diarrhoea with griping 
pains; in other cases the disease begins abruptly. An 
initial chill is rare. Diarrhoea is usually the first symptom. 
At first fecal and painless, the stools change their character 
within from twenty-four to thirty-six hours, becoming cha¬ 
racteristic of the disease. The dysenteric stools are first 
composed of mucus with a few scybalous fecal masses, but 
finally they consist only of mucus and blood (“ bloody 
slime ”). The presence of pus in the stools indicates fol¬ 
licular ulceration. The stools are frequent, varying from ten 
to two hundred in the twenty-four hours, and are small in 
quantity, rarely exceeding half an ounce. They are passed 
with a straining, bearing-down pain referred to the rectum. 
This tenesmus is more marked during and after a move- 


D YSENTER Y. 


499 


ment, but it may be more or less continuous, amounting to 
a constant desire to go to stool, and the patient may com¬ 
plain of burning pains referred to the rectum. Preceding 
each stool there is apt to be severe colicky pain in the abdo¬ 
men, with possibly some tenderness along the descending 
colon. The temperature is not high, varying from ioi° to 
103° F. at the outset. There are apt to be nausea and vom¬ 
iting with incessant thirst. Prostration may be extreme. 
Strangury may attend the rectal tenesmus, and in severe 
cases the urine may contain albumin and casts. As the patient 
improves the number of passages diminishes, the mucus be¬ 
comes opaque and less discolored by blood, and fecal matter 
begins to be passed. Rectal tenesmus finally disappears. 

2. If the inflammation involve the upper colon, and not the 
rectum, the clinical picture is different. The patient passes 
not mucus and blood, but large, watery, feculent stools with¬ 
out tenesmus. In severe cases blood may be admixed with 
the stools. Colicky abdominal pain precedes each passage. 
The constitutional symptoms are not severe, and the prog¬ 
nosis is that of the first form. In children this form is ac¬ 
companied by extreme prostration and febrile disturbance, 
so that the case may be mistaken for typhoid fever. 

The prognosis for the attack is good except in the ex¬ 
tremes of life. If the bowels can be opened within two days 
by castor oil, the attack will probably not be severe. It is 
possible for the disease to run into a chronic form. Peri¬ 
tonitis and abscess of the liver rarely occur. 

Diagnosis. —In children the disease may be mistaken for 
intussusception, while in adults cases of fecal impaction or 
of cancer of the intestine are frequently treated as dysentery 

Tropical or Amcebic Dysentery. 

Pathology.-—The amoeba coli or amoeba dysenteriae, a 
one-celled protoplasmic organism showing active amoeboid 


500 MANUAL OF THE PRACTICE OF MEDICINE. 

motion, is from io to 20 micromillimeters in diameter. It 
has been proven to be the inciter of dysentery in tropical and 
sub-tropical countries, and it is not uncommonly found in 
the Northern United States and in Europe. It probably 
gains access to the body by the medium of drinking-water. 
The large intestine is involved, particularly the descending 
colon, but the lower part of the ileum may also be affected. 
The lesion consists of oedema of the mucosa, with localized 
areas of cellular infiltration causing little elevations upon 
its surface. These elevations become necrotic and are cast 
off, exposing a yellowish-gray gelatinous mass which sub¬ 
sequently sloughs, leaving an ulcer with infiltrated and un¬ 
dermined edges extending through the submucosa and 
even to the serous layer of the colon. Extensive under¬ 
mining of the edges of the ulcerations allows of the forma¬ 
tion of fistulous tracts bridged over by apparently healthy 
mucous membrane. The colon may be so involved that 
the remaining mucous membrane projects like little islands 
from the surrounding ulcerations. The disease extends by 
progressive infiltration and ulceration of the mucous coat 
of the intestine, and in severe cases large areas may slough 
and be thrown off en masse. A croupous inflammation of 
the colon complicates amoebic dysentery in some cases. 
The microscope shows a notable absence of the products 
of purulent inflammation, but reveals amoebae in large num¬ 
bers in the floors and the walls of the ulcers. Healing of 
the ulcerations by cicatrization may lead to subsequent 
stricture of the intestine. One-fifth of the cases are com¬ 
plicated by lesions in the liver. There may be areas of necro¬ 
sis of the parenchyma of the liver, or there may be single or 
multiple abscesses, consisting of necrotic liver-tissue with a 
small amount of pus. Amoebae are constantly found in the 
contents of the abscesses. Rupture of an abscess of the liver 
into the right pleura or lung is not infrequent. 


D YSENTER V 


501 


Symptoms. —The onset of the disease is usually gradual, 
beginning as a diarrhoea; in severe cases, however, the dis¬ 
ease may begin abruptly. The temperature is but moder¬ 
ately raised, if at all. Pain and tenesmus may be present 
at the outset of severe cases, but they are not constant 
throughout the disease. The principal symptoms are diar¬ 
rhoea and a progressive loss of flesh and of strength. At 
the onset the stools may be mucoid and blood-stained as in 
catarrhal dysentery, but the characteristic stools are fluid, 
contain mucus and possibly blood, are of a yellowish-gray 
color, and in them are to be found actively moving amoebae. 
The number of the passages varies from six to twelve in the 
twenty-four hours. The diarrhoea runs an irregular course 
of from four to eight weeks, with periods of temporary im¬ 
provement. 

Prognosis. —Recovery is usually slow and tedious from 
anaemia and muscular weakness, and convalescence may be 
interrupted by relapses. The disease has a greater mortality 
than catarrhal dysentery, and shows a tendency to become 
chronic. Death may result from the severity of the local 
inflammation, from exhaustion in the prolonged cases, or 
by reason of the liver complications. 

Acute Croupous Dysentery. 

This form of dysentery may occur in a primary form or 
may appear as a terminal complication of chronic heart dis¬ 
ease, of chronic Bright’s disease, of profound cachectic 
states, or of lobar pneumonia. 

Pathology. —The colon is thickened and infiltrated by 
fibrin, serum, and pus-cells, so that the mucosa, from the 
ileo-caecal valve to the rectum, appears as a yellowish exu¬ 
date without trace of glandular structures. In mild cases 
the tops of the folds of the colon are covered with a thin 
yellowish or grayish pellicle. The mucosa thus infiltrated 


502 MANUAL OF THE PRACTICE OF MEDICINE. 

undergoes necrosis, and sloughs, leaving laige irregular 
ulcers which may involve the submucosa and even the mus¬ 
cular wall. Perforation of the ulcers is not uncommon. In 
some cases the lower portions of the colon alone are in¬ 
volved. Peritonitis may complicate the disease even with¬ 
out actual rupture, and ulcer of the liver may result from 
infective thrombosis of one of the mesenteric veins. Should 
the patient recover, the ulcerations will cicatrize and stric¬ 
ture of the intestine may result ; but the healing of the 
ulcers is very slow, and in many cases chronic ulcerations 

are left. 

The symptoms of acute croupous dysentery resemble 
those of the catarrhal form, but are more severe. If the 
rectum be involved, tormina and tenesmus are extreme, the 
stools are numerous, are composed of mucus, blood, pus, 
and shreds of sloughing membrane, the temperature is 
high, prostration is extreme, and the patient is seriously ill 
from the onset. If the rectum be not involved, there is no 
tenesmus; the stools are diarrhoeal in character, contain 
blood, pus, and shreds of membrane, and are accompanied 
by severe abdominal pain. The constitutional symptoms 
are severe, closely resembling those of typhoid fever. 

In the secondary cases the patient is already ill from the 
primary disease, so that the course of the dysentery is in¬ 
sidious. There is usually a moderate diarrhoea, with the 
occasional passage of blood and mucus. 

The prognosis of croupous dysentery is exceedingly 
grave. Death may result from the severity of the inflam¬ 
mation, from peritonitis or perforation, or from abscess of 
the liver ; or the patient may pass into the typhoid condi¬ 
tion or may die exhausted. Should the patient recover 
from the acute attack, the condition may become chronic. 

Complications. —The course of the disease may be com¬ 
plicated by septic arthritis, endocarditis, pericarditis, pleu- 


D YSENTER V 


503 


risy, and pyaemia. Peripheral neuritis with paraplegia is 
a rare complication. The occurrence of pylephlebitis and 
abscesses in the liver has already been alluded to. Chronic 
nephritis has in some cases followed the disease. 

Treatment of Acute Dysentery. 

Of the Catarrhal Form .—The patient should be put to 
bed, no matter how trifling the attack may seem, and should 
be kept on a milk or liquid diet. It is important that the 
bowels should be moved at the beginning of the attack, 
castor oil being the preferable laxative. An estimate of the 
probable duration can often be made with reasonable accu¬ 
racy by the promptness of the response to the laxative 
remedies. The bowels should be opened every second day, 
if possible. Opium should be given by the mouth or by 
suppository, to control the tormina and the tenesmus. 
Much relief is often afforded by rectal medication. An 
enema of hot starch-water containing from 10 to 15 
drops of laudanum may be given after every passage. As 
the enemata are seldom retained for any length of time, 
poisoning is not likely to occur. Suppositories containing 
grain of cocaine hydrochlorate, or injections of from 5 to 
10 drops of a 4 per cent, solution of the drug, are ser¬ 
viceable in mitigating the pain, but the absorptive power 
of the rectum is so great that toxic symptoms may occur 
unless the case is watched with care. Quinine (gr. x-xv 
daily) should be given if there be a malarial history. Bichlo¬ 
ride of mercury (gr. may be given every two hours, 
and large doses of bismuth subnitrate (%] q. 2 h.) are often of 
great service. Astringent rectal injections are not recom¬ 
mended in acute cases. 

In severe cases ipecacuanha may be given in large doses. 
This drug, without doubt, is of great service, especially in 
the cases occurring in the tropics. A hypodermic injection 


504 MANUAL OF THE PRACTICE OF MEDICINE. 

of morphine should be given, followed in half an hour by 
from 20 to 40 grains of powdered ipecacuanha in capsule. 
A second injection of morphine should be given if vomiting 
threaten. No food should be given for six hours after the . 
dosage. If vomiting occur, the dose may be repeated with¬ 
in a few hours. 

Amoebic Dysentery .—Besides the above-mentioned treat¬ 
ment, colon-irrigation of quinine (1 : 2500) may be used, 
the amoebae being rapidly killed by the drug. Medication 
should be continued in these cases until the amoebae are no 
longer present in the stools. 

For croupous dysentery the treatment is that of the ca¬ 
tarrhal form, except that opium is required in larger 
doses, and stimulants are needed to support the strength 
of the patient. Should extensive ulceration exist, purga¬ 
tives must be administered with caution. 

Chronic Dysentery. 

Etiology.—Chronic dysentery may be chronic from the 
first or may succeed an acute attack. Many cases of 
amoebic dysentery may be subacute from the start. 

Pathology.—The mucosa is thickened, pigmented, and 
presents an irregular puckered surface. The submucosa 
and the muscular coats are usually hypertrophied, and the 
lumen of the colon may be diminished. Cystic degenera¬ 
tion of the glandular structures may be visible to the naked 
eye. Ulcerations are generally present in all stages of 
development; they are usually pigmented. 

Symptoms.—Tormina and tenesmus are uncommon 
unless during acute exacerbations. The stools vary from 
three to fifteen in the twenty-four hours, and are not always 
of the same character; they may be composed of mucus, 
occasionally stained with blood, or they may be liquid and 
frothy, consisting of feces, mucus, and undigested food. 


APPENDICITIS. 


505 


Blood and shreds of tissue are not common except during 
the acute exacerbations. There may be constipation alter¬ 
nating with diarrhoea. From time to time will appear acute 
exacerbations in which the stools assume a more character¬ 
istic appearance of dysentery and are accompanied by tor¬ 
mina and tenesmus. Pain and tenderness along the colon 
are usually present. 1 he patient rapidly loses flesh and 
strength ; the tongue resembles raw beef; digestion is inter¬ 
fered with; flatulence is common; anaemia and emaciation 
reach finally an extreme degree. 

Prognosis. —The course of chronic dysentery is pro¬ 
longed for months or possibly for years, the patient usually 
dying from exhaustion and inanition. 

Treatment.—Proper diet is of prime importance. The 
patient should be put to bed and be given a milk diet. 
Should curds appear in the stools, meat broths or scraped 
beef may be given, and only such food be allowed as may 
be digested thoroughly. Inspection of the stools should 
then govern the diet. Colon-irrigation should be employed 
daily, simple salt-solution (zj : Oj) being the preferable solu¬ 
tion. Medicated and astringent injections are painful, and 
are not more efficacious than simple cleansing solutions. 

APPENDICITIS. 

Etiology.—Appendicitis is more common in the young 
than in the old, one-half the cases occurring before the 
twentieth year. Males are affected in three-fourths of the 
cases. In a little less than half the cases hard fecal con¬ 
cretions or foreign bodies, such as grape-seeds, orange-pips, 
etc., are found in the diseased appendix ; on this point, how¬ 
ever, statistics are misleading, the percentage of cases in 
which concretions are found being estimated as low as 6 
per cent, by some observers, while the concretions are said 
to be present in 10 per cent, of presumably healthy appen- 


506 manual of the practice of medicine. 


dices. The question as to whether foreign bodies and con¬ 
cretions can originate an attack of appendicitis is still un¬ 
answered. It would seem, however, that foreign bodies,. 
concretions, exposure to wet and cold, injury and over¬ 
straining, and previous inflammations of the appendix or 
the narrowing of its lumen by stricture or by twists, render 
the appendix more susceptible to the infection of micro¬ 
organisms, so that they may be considered as causes pre¬ 
disposing to a bacterial infection. 

Acute Catarrhal Appendicitis. 

Pathology.—The mucous membrane lining the appendix 
is in a condition of catarrhal inflammation ; the walls are 
swollen and are infiltrated by serum and leucocytes, so that 
the appendix is enlarged and its lumen becomes contracted, 
especially toward the caecal end. The peritoneum covering 
the appendix is congested, is coated with fibrin, and is ad¬ 
herent to neighboring peritoneal surfaces. In this, the mild¬ 
est and commonest form of appendicitis, there is no general 
peritonitis, no abscess, and no perforation. 

Symptoms may begin gradually or suddenly. If gradu¬ 
ally, there is a preliminary diarrhoea, or diarrhoea alternating 

with constipation, and a pain which 
is either of a colicky character or 
is localized in the right iliac fossa. 
Cases with a sudden onset are in¬ 
itiated by a chill or by chilly feel¬ 
ings. When the disease has de¬ 
veloped there is fever, usually of 
moderate intensity, running be¬ 
tween ioi° and 103° F., remain¬ 
ing for three or four days and 
It is of the greatest importance to 
accurate records of the temperature of each patient, 



Fig. 43. —Catarrhal appendicitis : 
localized fibrinous peritonitis; no 
pus-formation; no general peri¬ 
tonitis. 

then slowly subsiding. 



APPENDICITIS. 


50 7 


as it is impossible at the onset to distinguish between the 
mild and the severe forms, and the exact diagnosis, the 
presence of complications, and the indications for operative 
interference are all determined, in great measure, by the 
character of the temperature curve. With the fever there 
are headache, loss of appetite, nausea and vomiting, and 
prostration. 

Local symptoms consist of pain, tenderness, and position 
in bed. 

Pain , which is localized in the right iliac fossa, may be 
steady or paroxysmal. Should the appendix be abnormally 
situated, the pain may be felt in the right lumbar region or 
nearer the median line in front. In some cases the pain 
cannot accurately be localized. 

Tenderness is usually elicited by firm continuous pressure 
at McBurney’s point, situated from one and a half to two 
inches from the right anterior superior spine, on a line 
drawn between this bony prominence and the umbilicus. 
If the appendix be displaced behind the caecum, tenderness 
may not be elicited at McBurney’s point, but may be de¬ 
tected by vaginal or rectal examination ; hence, in doubtful 
cases, these methods of examination should always be re¬ 
sorted to. The thigh is usually flexed to relax the anterior 
abdomen; it may be adducted from irritation of the obtu¬ 
rator nerve within the pelvis. 

Physical Examination. —Tenderness is produced by pres¬ 
sure at McBurney’s point or by rectal or vaginal examination. 
There is usually considerable rigidity of the abdominal wall 
in the right iliac region. There may be a feeling of resist¬ 
ance in the right iliac region, and slight dulness on percus¬ 
sion, but no defined tumor can be appreciated. The detec¬ 
tion of resistance and dulness on percussion depend upon 
the position of the vermiform appendix (not being appre¬ 
ciable should the appendix be behind the caecum) and upon 


508 manual of the practice of medicine . 


the extent of the localized peritonitis. Should several coils 
of intestines be matted together and adherent to the appen¬ 
dix, the resistance and dulness may be as well marked as in 
cases of the suppurative form. 

Course of the Disease.—After from two to four days 
the patient begins to improve, showing that the case is one 
of the mild form, and in about a week convalescence is 
thoroughly established. Pain, tenderness, and irregular 
action of the bowels may, however, persist for some weeks, 
owing to the resulting peritoneal adhesions, and relapses 
may occur at any time. 

Acute Suppurative Appendicitis (Ulcerative 

Appendicitis). 

Pathology.—In this form of appendicitis the wall of the 
appendix is infiltrated by fibrin, serum, and pus, and in 
severe cases the wall may slough in some part, so that the 

contents of the appendix escape 
into the peritoneum. The ad¬ 
jacent peritoneal surfaces are 
inflamed, coated with fibrin and 
pus, and become adherent, so 
that there is formed a cavity 
containing pus. This circum¬ 
scribed intraperitoneal abscess 
may remain localized or may 
rupture into the general peri¬ 
toneal cavity, producing acute 
peritoneal septicaemia; or diffuse suppurative peritonitis 
may result without actual rupture. Suppuration may ex¬ 
tend along the connective tissue in the mesentery of the 
appendix and invade the retroperitoneal tissues. This for¬ 
mation of an extraperitoneal abscess is not common, and 
occurs only in connection with the intraperitoneal abscess 



Fig. 44. —Suppurative appendicitis: 
limiting adhesions; localized intra¬ 
peritoneal abscess. 


APPENDICITIS. 


509 

previously described (Figs. 44, 45). The peritoneum divid¬ 
ing the inti aperitoneal from the extraperitoneal abscess ulti¬ 
mately becomes absorbed, so that one large abscess-cavity 
results. 

The pus may be abundant and creamy, or the quantity 
may be small and surrounded by a large amount of inflam¬ 
matory tissue. The pus is usually 
grayish in color, exceedingly offen¬ 
sive, and, should sloughing of the 
vermiform appendix occur, may be 
admixed with the contents of the in¬ 
testine. Bacterial examination usu¬ 
ally reveals pure cultures of the ba¬ 
cillus coli commune. 

1 he position of the abscess varies 
according to the position of the ap¬ 
pendix. The usual situation is in the 
angle of the ileum and the caecum, 
lying on the psoas muscle. In other 
cases the abscess lies behind the cae¬ 
cum or extends into the pelvis. 

Rupture of the abscess may occur 
at any time, either into the perito¬ 
neum, the intestine, or the bladder, 
or, less frequently, through the abdominal wall, the pleura, 
the portal vein, or the iliac artery. When the retroperito¬ 
neal tissues become infected, the so-called “ perityphlitic ” 
abscess may burrow under the iliac fascia and appear below 
Poupart’s ligament, or may extend to the perinephritic tis¬ 
sues. Suppuration may extend along the psoas fascia or 
may involve the perirectal connective tissue. Burrowing 
through the obturator foramen, the pus may appear as a 
gluteal abscess. 

The symptoms begin like those of the catarrhal form, 



Fig. 45. —Cross-section of 
appendix with suppurative 
inflammation, showing ex¬ 
tension of the infection along 
the connective tissue of the 
mesentery to the retroperi¬ 
toneal connective tissue, and 
the formation of an extra- 
peritoneal abscess. The 
peritoneum separating the 
intraperitoneal from the ex¬ 
traperitoneal suppuration is 
here shown intact; it, how¬ 
ever, subsequently disap¬ 
pears. 





510 MANUAL OF THE PRACTICE OF MEDICINE. 

but they are more severe. The temperature ranges between 
102° and 104° F.; pain and tenderness are well marked; 
the thigh is flexed and adducted; the bladder and the 
rectum may give evidences of irritability. 

The physical signs during the earlier stages of the dis¬ 
ease depend upon the position of the abscess. 

(a) If the abscess be in the inner side or in front of the 
caecum, there will be tenderness in the right iliac fossa, 
especially marked over McBurney’s point. There may be 
some bulging in the right iliac fossa, in which region a 
percussion-note of dulness is obtained. The abdominal wall 
on the right side is rigid, and there is an indistinct tender 
mass to be felt in the region of the appendix. 

( b ) If the abscess be small and be situated behind the 
caecum and the distended intestines, tenderness on palpation 
will be elicited, but no tumor can be detected, although 
there may be a sense of resistance to palpation. The per¬ 
cussion-note is tympanitic, and some oedema may be noticed 
in the right lumbar region. 

(y) If the abscess encroach upon the pelvic space, the 
physical signs may not be elicited by external abdominal 
examination, but rectal or vaginal examination detects the 
presence of the abscess. 

Instead of the disease subsiding in three or four days, as 
does the catarrhal form, the symptoms become aggravated. 
The temperature becomes irregular and remittent, and septic 
symptoms appear on the third or fourth day and are strik¬ 
ingly developed by the end of the first week. In some 
cases there are added the symptoms of intestinal obstruc¬ 
tion from septic paralysis of the intestinal wall. 

Physical examination by the seventh or tenth day may 
reveal, by palpation through the abdominal wall, the rectum, 
or the vagina, an indistinct wave of fluctuation in the tumor- 
mass. The fluctuation is most marked in extraperitoneal 


APPENDICITIS. 


5 11 

abscesses, and is detected above Poupart’s ligament or above 
the crest of the ilium. The abscess may, however, be small, 
and may be in a locality where it cannot be felt, so the 
diagnosis may still be doubtful. The aspirating-needle 
should never be used for diagnostic purposes unless a 
marked tumor with dulness is present in the cmcal region, 
and even then it should be used with extreme caution. 

Course of the Disease.— i. Some patients gradually re¬ 
cover. The temperature declines, pain and tenderness sub¬ 
side, and the physical signs clear up. These are the cases 
of mild infection in which the peritoneal exudate is chiefly 
fibrino-serous without much admixture of pus, so that 
absorption of the effusion is possible. 

2. Other cases go on with the symptoms of sepsis and of 
a localized peritoneal abscess. 

(a) Some cases are operated upon and the pus is evacu¬ 
ated. 

(/;) In some cases the abscess ruptures. If the rupture 
occur through the abdominal wall or into the bladder, the 
rectum, or the intestine, the pus will appear externally, the 
temperature will fall, and the general symptoms will im¬ 
prove. If drainage be good, a spontaneous cure will result, 
but if drainage be poor, the abscess-cavity will fill up again 
and the old symptoms will reappear. Fistulse may result, 
and there may be a resulting cystitis which, if the bladder 
be perforated, may prove fatal. 

(c) Burrowing may occur, so that pus will rupture into 
distant parts, even into the pleural cavity. 

( d ) Acute progressive peritonitis may develop. This is 
the greatest danger, and usually begins in the second, 
third, or fourth day, before the limiting adhesions have 
become firm enough to prevent general infection of the 
peritoneum. Spreading abdominal pain, tympanites, and 
an increase in all the constitutional symptoms indicate 


512 MANUAL OF THE PRACTICE OF MEDICINE. 


the onset of the peritonitis. In some cases there is a pro¬ 
gressive increase in the size of the tumor. 







'W 



Day of 
Disease 

1 

2 

3 

4 




107° 

106° 

105° 

104° 

103 c 

102° 

101° 

100° 



























• 


























: 


























£ 


























y, 


























/ 


















N 
































\ 


/ 








































































Fig. 46. —Suppurative appendicitis: rupture of abscess into peritoneal cavity; acute 

peritoneal sepsis. 

(e) The abscess may rupture and discharge its contents 
into the peritoneal cavity, so that acute peritoneal sepsis 
may result. The temperature falls, but subsequently rises 
to a higher point than before, and collapse symptoms appear. 
Death may occur in from twelve to fifteen hours from col¬ 
lapse, with high ante-mortem temperature, or the symptoms 
of a general peritonitis will develop from which the patient 
will die in two or three days (see Fig. 46). 

3. The course of the disease may be modified by compli¬ 
cations. Among these may be mentioned thrombosis of 
the femoral vein, and thrombosis of the portal vein which 
may be infective, leading to pyaemia with multiple abscesses 
in the liver. Pyaemia or septicaemia may develop in neglected 
cases. 





















































APPENDICITIS. 


513 


Gangrenous Appendicitis. 

Under the above heading are included the rather rare 
cases in which primary gangrene or necrosis of the appen¬ 
dix-wall occurs, so that the contents of the appendix are 
discharged into the peritoneal 
cavity before there is time for 
limiting peritoneal adhesions to 
be formed. The patient usually 
has suffered from previous at¬ 
tacks of catarrhal or suppurative 
appendicitis, with resulting ad¬ 
hesions, so that the appendix 
becomes distorted and twisted. 

Usually the exciting cause is a 
foreign body or a fecal concre¬ 
tion which enters the appendix 
and induces a pressure-necrosis on its wall. There maybe a 
local peritonitis, but no adhesions are formed, so that the 
sloughing appendix lies free in the peritoneal cavity. Acute 
peritoneal sepsis develops, and usually runs a fatal course. 

The symptoms begin like those of the suppurative form, 
but the patient is evidently more sick. Peritoneal sepsis 
and death usually result before a tumor can be appreciated. 



Fig. 47. —Gangrenous appendicitis ; 
sloughing of the wall; escape of con¬ 
tents into peritoneal cavity ; absence 
of limiting adhesions. 


Prognosis of Appendicitis. 

In the catarrhal form the prognosis is good. It should 
be remembered, however, that the appendix is left adherent 
and predisposed to recurrent attacks. 

In the suppurative form the prognosis is exceedingly 
good, depending less, however, upon the intensity of the 
inflammation than upon the skill of the surgeon. When 
general peritonitis occurs the prognosis is most unfavorable. 
Rupture of the abscess into the general peritoneal cavity 
33 


514 MANUAL OF THE PRACTICE OF MEDICINE. 

is almost regularly fatal. Spontaneous cure may occur by 
absorption or by perforation through the abdominal wall 
or into the bladder or the rectum, but aside from these 
cases the prognosis is bad unless the case be treated sur¬ 
gically and the abscess-cavity be drained. 

Gangrenous appendicitis , unless operated upon very early 
in the course of the disease, before actual perforation has 
occurred, is rapidly fatal. 

, f ^ . 

Treatment of Appendicitis. 

*S.\ \_ 

No disease requires more judgment for its proper treat¬ 
ment than appendicitis, as no routine plan of treatment is 
applicable to all patients. In every case a surgeon should 
be called into consultation, as the disease is, properly speak¬ 
ing, a surgical one. The treatment is both medical and 
surgical. 

Medical Treatment .—The patient should be put to bed, 
no matter how mild the case may appear, and be put upon 
a liquid diet. Opium is to be given, to quiet the patient 
and to allay pain, but large doses to the point of semi¬ 
narcotization are not to be recommended. Cathartics are 
absolutely contraindicated, because of the danger of ruptur¬ 
ing limiting peritoneal adhesions by the increase of intes¬ 
tinal peristalsis. The bowels should, however, be moved 
every second day by enemata of tepid water containing salt 
(3j : Oj). An ice-bag should be applied to the Ccxcal region, 
or a Leiter cold coil may be used. Hot poultices are not 
recommended. 

Surgical treatment consists in evacuation of the pus, 
removal of the diseased appendix, and drainage of the ab¬ 
scess-cavity. 

Operative interference is indicated under the following 
conditions: (i) In catarrhal appendicitis with severe con¬ 
stitutional symptoms, especially if the attack be recurrent; 


APPENDICITIS. 


515 

(2) whenever symptoms of pus-absorption are present, 
whether the tumor can be felt or not ; (3) whenever the 
patient is more than ordinarily sick, and does not seem to be 
standing the disease well; (4) should septicaemia develop; 
(5) in cases of spreading peritonitis; (6) in case of rupture 
and peritoneal sepsis; (7) in case of burrowing of the ab¬ 
scess; (8) in all cases in which a tumor presents itself; (9) 
in case of rupture into the bladder, the intestine, or the 
rectum, the drainage being imperfect. 

Chronic Appendicitis. 

This form of appendicitis occurs in patients who have had 
previous attacks of acute inflammation of the appendix. 

Pathology.— The appendix is usually enlarged and of a 
sausage shape. Its walls are thickened, the outlet is ste- 
nosed, and its cavity is filled with mucus. The appendix 
may be sharply bent upon itself or displaced. The peri¬ 
toneum adjacent to the appendix is thickened and adherent. 
There may be collections of serum or of sero-pus encapsu¬ 
lated by the peritoneal adhesions. 

Symptoms.— In some cases there are recurring attacks 
of acute appendicitis, in the intervals of which the patient 
is perfectly free from trouble. To these cases the name 
“ recurring appendicitis ” is frequently applied. 

In other cases the patient suffers more or less in the 
intervals from the chronic inflammation of the appendix; to 
these cases the terms “ chronic appendicitis ” and “ chronic 
relapsing appendicitis ” are more properly applied. 

The symptoms between acute attacks consist of localized 
pain and tenderness, disturbances of digestion, and irregular 
action of the bowels. There is usually progressive loss of 
flesh and strength. Physical examination usually reveals 
tenderness over McBurney’s point, a tumor or a sense of 
resistance, and a dull tympanitic note on percussion. 


5 l6 MANUAL OF THE PRACTICE OF MEDICINE. 

The symptoms of the acute exacerbations resemble those 
of the primary attack. These acute exacerbations may 
occur at any time, so that the patient becomes afraid to 
travel from home, being apprehensive of the increasing 
severity of future attacks, or may become unable to pur¬ 
sue business or laborious occupation. 

The duration of the disease varies from one to ten years; 
the acute attacks vary in number from two to twenty or 
thirty. 

The prognosis depends upon the character of each acute 
attack. 

The treatment is surgical. The question whether to 
operate during an interim or to wait until the symptoms 
of an acute attack call for surgical interference should be 
left to the surgeon to decide upon the merits of each indi¬ 
vidual case. 

ULCERATION OF THE INTESTINE. 

The following intestinal ulcerations may be described: 

I. Round ulcer of the duodenum resembles gastric ulcer 
in its cause and appearance, but is much less common 
(as 40 to 1). The ulcer is usually single and situated near 
the pylorus. Localized peritonitis with adhesions, local¬ 
ized peritoneal abscess, perforative peritonitis, and hemor¬ 
rhage are the most frequent complications, while stenosis 
of the pylorus, of the orifices of the common bile-duct, 
or of the pancreatic duct may result from cicatricial con¬ 
traction. 

The symptoms closely resemble those of gastric ulcer. 
Pain is referred to the right hypochondrium, is rarely severe, 
and appears later after eating than does the pain of gastric 
ulcer. There may be only irregular, ill-defined feelings re¬ 
ferred to the hypochondrium, with localized tenderness. 
Dyspeptic symptoms and vomiting are exceedingly rare. 


ULCERATION OF THE INTESTINE. 


5 1 7 

orrha^e occurs in one-third of the cases. The blood 
may be vomited or be passed in an altered condition by the 
bowel, oi the patient may die before the blood has time to 
appear externally. Many cases run a latent or obscure 
couise, and in these cases death from hemorrhage or from 
perforation may be the first indication of serious disease, 
although in the latter case severe continuous pain usually 
precedes the rupture by several days. 

The prognosis is more serious than that of gastric ulcer. 

The treatment is that of ulcer of the stomach. 

2. Duodenal ulceiation may occur after extensive burns 
of the skin. The duodenum is congested and ulcerated in 
patches of an irregular form, the lesions appearing in from 
seven to fourteen days after the injury. The exact patho¬ 
genesis of these cases is unknown. Hemorrhage and per¬ 
foration are the chief symptoms, and the patient almost 
invariably dies. 

3. Embolic ulcers may result from embolism or throm¬ 
bosis of a branch of the mesenteric artery. The emboli 
may arise from endocardial vegetation or from atheroma of 
the aorta, while the occurrence of thrombus is favored by 
atheroma of the mesenteric artery itself. The mesenteric 
vessels being terminal arteries, embolism or thrombosis 
leads to hemorrhagic infarction of a section of the intestinal 
wall, which rapidly undergoes necrosis. The peritoneum 
over the affected area is inflamed and may be the seat of 
perforation, and the intestine itself in the vicinity is con¬ 
gested and infiltrated with blood. The diagnosis is to be 
made by attention to the following points : (1) The presence 
of a cause for embolism ; (2) the presence of emboli in other 
organs; (3) symptoms of intense enteritis; (4) symptoms 
of peritonitis. If the embolus be septic, extensive suppu¬ 
ration of the intestinal wall will result. Embolic ulcers of 
the colon are exceedingly rare. 


5 1 8 MANUAL OF THE PRACTICE OF MEDICINE. 

4. Ulcers due to amyloid degeneration may be found in any 
part of the intestinal tract, being due to local disturbances 
of nutrition consequent upon the diminished supply of blood 
that necessarily results from the waxy changes in the wall 
of the terminal arteries. These ulcers show no disposition 
to heal. 

5. Catarrhal and follicidar idcers result from acute and 
chronic enteritis. Catarrhal ulcers are usually found in the 
colon, either as slight erosions or involving large areas by 
their extension and confluence. The floor and the walls of 
long-continued ulcers become greatly thickened. The natu¬ 
ral termination is by cicatrization. 

Follicular ulcers may be found in either the large or the 
small intestine. They are of round shape, with undermined 
edges. They may be so numerous that the bowel is studded 
by them. Follicular ulcers may extend by ulceration of 
neighboring parts or may perforate. Cicatrization seldom 
results if the lesion be extensive. 

6. Stercoral Ulcers. —The pressure of hardened feces leads 
to necrosis and subsequent purulent infiltration of the mu¬ 
cosa. Stercoral ulcers occur in situations in which fecal 
accumulation is liable to occur, as in the caecum, the rectum, 
the flexures of the colon, or above the point of stricture in 
intestinal obstruction. 

7. The ulcers of typhoid fever, diphtheria, variola, and 
anthrax have elsewhere been described. 

8. Tubercidar ulcers are of common occurrence. They may 
appear as a primary infection from the ingestion of tubercu¬ 
lar meat or milk, especially in children, but they are more 
common as the result of secondary infection complicating pul¬ 
monary or genito-urinary tuberculosis. The process begins 
first in the ileum, extending thence to the rest of the small 
and the large intestine. Tubercles first develop in the 
solitary or agminated follicles, undergo cheesy degeneration, 


ULCERATION OF THE INTESTINE. 


519 


and break down to form ulcers. These follicular ulcers 
extend by suppuration and by extension of tubercular de¬ 
posits along the line of the lymphatic vessels, so that 

girdle ulcers are formed, encircling the intestine at right 
angles to its long axis. The peritoneum covering the site 
of the ulcer is studded with tubercles, is coated with fibrin, 
and is adherent to adjacent surfaces. Perforation may 
occur; it is usually prevented, however, by the formation 
of peritoneal adhesions. The mesenteric glands are al¬ 
most invariably enlarged and tubercular. The girdle 
shape of the ulcer distinguishes it from typhoid ulcera¬ 
tion. A differential diagnosis in the earlier stages can be 
made by the fact that in typhoid fever ulceration of a Peyer’s 
patch is uniform, whereas in tubercular disease separate 
follicles are involved, while others entirely escape. Cicatri¬ 
zation is rare, but it is possible. 

9. Leukmnic ulcers result from necrosis of lymphoid de¬ 
posits in the wall of the intestine. They are rare, however, 
except during the course of acute leukaemia. 

10. Scorbutic ulcers may follow hemorrhages into the 
mucosa. 

11. Syphilitic ulcers are rare in the small intestine except 
in new-born syphilitic children. Gummata of the intes¬ 
tinal wall may occur, and ulcers may result from their 
breaking down. Syphilitic ulceration of the rectum is not 
uncommon, especially in women; it leads to progressive 
fibrous stricture. 

12. Urcemic ulcers may occur with advanced nephritis in 
several ways : (a) Ulceration of solitary and agminated folli¬ 
cles, with catarrhal entero-colitis ; (b) as a result of a pseudo¬ 
membranous enteritis; (c) gangrenous ulceration may 
occur. 

13. Mercurial tilcers follow pseudo-membranous enteritis 
from poisoning by mercury. 


520 MANUAL OF THE PRACTICE OF MEDICINE. 

14. Cancerous ulcerations may result from the breaking 
down of submucous nodules. 

15. Ulceration from external perforation may occur from 
ulceration and erosion of new growths or by the perforation 
of a neighboring abscess into the intestine. 

The symptoms of ulceration of the intestine depend upon 
the position and extent of the ulceration and upon its patho¬ 
logical character. 

Diarrhoea is a frequent symptom, being regularly present 
with ulcers of the lower portion of the colon and the upper 
portion of the rectum. Ulcers limited to the small intestine, 
the caecum, and the ascending colon do not of themselves 
cause diarrhoea. 

Hemorrhage varies in amount, the largest hemorrhages 
occurring with duodenal ulceration, typhoid fever, and per¬ 
foration from without the intestine. If the origin of the 
hemorrhage be in the upper portion of the intestine, the 
blood is usually dark and altered and mixed with feces: 
hematin-crystals may alone be detected. 

Pus in the stools is rare unless from ulceration, and hence 
its presence is of great diagnostic importance. Large evacu¬ 
ations of pus indicate rupture of a neighboring abscess into 
the intestine. Usually the quantity of pus is small, necessi¬ 
tating for its detection close scrutiny, and even microscopical 
examination, of the feces. Pus with blood and mucus usu¬ 
ally indicates dysentery or an ulcerating carcinoma of the 
colon or the rectum. Shreds of tissue, if proven not to con¬ 
sist of undigested food, afford conclusive proof of rapid and 
extensive ulceration. Tubercle bacilli in the stools are 
usually, but not invariably, found in cases of tubercular 
ulceration. 

Pain is frequently absent. It may be of the nature of a 
colic, or there may be steady pain due to a complicating 
localized peritonitis. Tenderness, which may be constant 


CANCER OF THE INTESTINE. 


521 


over a small area, is of value in localizing the seat of ulcera¬ 
tion. Tenesmus occurs only if the rectum be ulcerated. 

Fever depends upon associated conditions. Emaciation 
depends upon the extent and pathological character of the 
ulcers, and is more pronounced when the small intestine is 
affected. 

Not infrequently ulcers of the intestine run an entirely 
latent course, and are unexpectedly found at post-mortem 
examination. 

The complications of ulceration comprise localized peri¬ 
tonitis, peritoneal abscess, purulent or perforative peritonitis, 
and hemorrhage; should cicatrization occur, intestinal ob¬ 
struction may result. 

Treatment. —The diet should be easily digestible, nutri¬ 
tious, and unirritating. A milk diet is indicated in severe 
cases, and prolonged rest in bed may be necessary to accom¬ 
plish good results. For ulceration of the small intestines 
antiseptics by the mouth should be given, to keep the intes¬ 
tinal tract disinfected so far as possible. Bismuth salicylate 
and subnitrate (each 15 grains every three or four hours) 
are of great value, but salol, bismuth subgallate, naphthalin, 
and resorcin may be used. For ulceration of the colon 
large injections of warm salt-solution are to be given to 
cleanse the bowels. The addition of astringent or irritating 
drugs, such as nitrate of silver, salicylic acid, or thymol, 
does not seem to increase the medicinal value of these in¬ 
jections, and certainly renders them painful and annoying. 

Ulceration of the rectum can be treated, if within reach, 
by the methods pursued in treating external ulcers. 

CANCER OF THE INTESTINE. 

Carcinoma of the intestine usually occurs as a primary 
growth, and comprises from 4 to 8 per cent, of all cases 
of cancerous disease. Four varieties are encountered: 


522 MANUAL OF THE PRACTICE OF MEDICINE. 

scirrhus, encephaloid, colloid, and the cylindrical-celled 
epithelioma. Growths in the large intestine are nine times 
as common as those of the small intestine, the seats of selec¬ 
tion being the rectum (80 per cent, of all intestinal cancers), 
the sigmoid flexure, and the caput coli. Next in frequency 
comes cancer of the duodenum. 

Pathology.—Scirrhus usually produces a hard infiltra¬ 
tion of the intestinal wall, narrowing the lumen of the gut. 
The encephaloid and cylindrical-celled epithelioma form 
annular constrictions, large fungoid masses projecting into 
the cavity of the intestine, and are very prone to ulceration 
and hemorrhage. The colloid form produces a gelatinous 
infiltration of the intestinal wall, without much tendency to 
ulcerate or to cause obstruction. Secondary deposits are 
not uncommon, especially in the liver, the general rule be¬ 
ing that when secondary cancer of the liver develops, the 
primary cancer in the intestine ceases to grow and often 
gives no further symptoms, so that the case will resemble 
one of primary cancer of the liver. 

from the ulceration of the cancer perforation may occur 
into the peritoneum or into hollow viscera, forming fecal 
fistulae ; or extensive hemorrhage may result. The intestine 
becomes more or less occluded, the obstruction beine often 

o 

rendered more complete by fecal accumulation at the point 
of stricture. 

Cancer of the Rectum. 

Symptoms.—Pain is usually more marked than that pro¬ 
duced by cancer in any other part, excepting cancer of the 
tongue. The pain is not always of the same kind, (a) In some 
cases the pain is the same as that produced by cancer in any 
other part of the body—dull, boring, and continuous, (fr) The 
pain may be neuralgic, and is due to pressure on the sacral 
plexus. These cases are frequently treated for sciatica. 


CANCER OF THE INTESTINE . 523 

(f) The pain may be due to obstruction of the rectum, 
being paroxysmal and straining in character. These 
cases are often treated for chronic dysentery or for fecal 
impaction. 

Hemorrhage is usually in small amounts; it is brought 
on by straining attempts at stool. Occasionally, however, 
the bleeding is profuse. 

In nearly all cases there is an irritating discharge which 
excoriates the anus and the neighboring parts. Should the 
sphincter ani be relaxed, as often happens, the condition of the 
patient is rendered more uncomfortable. There are regularly 
changes in the action of the bowels : ( a ) There may be diar¬ 
rhoea accompanied by pain and tenesmus ; (Jj) the stools may 
be deformed by being forced through the constricted rectum, 
so as to be ribbon-shaped or as small in diameter as a lead- 
pencil ; (o) there may be constipation with symptoms of 
intestinal obstruction. Should the obstructing growth 
ulcerate, the constipation will suddenly give way. Cancer¬ 
ous cachexia intervenes, and the symptoms of secondary 
deposits in adjacent viscera or in the liver may complicate 
the latter stages of the disease. 

Physical Examination.—There may be a hard ring felt 


ABC D E F 



Fig 48. —Physical examination of cancer of the rectum. 


two or three inches from the anus, usually just large enough 
to admit the finger (Fig. 48, a). In some cases the 
bowel is invaginated, so that the ring is pushed down by 





524 MANUAL OF THE PRACTICE OF MEDICINE. 

the accumulation of feces above (b), and the orifice of the 
constriction may be tilted so that it is found with difficulty 
(c). In either case there are felt projecting into the rec¬ 
tum large friable masses which bleed readily (d), or ulcera¬ 
tions with hard edges and floor may be detected (e). In 
cases of colloid carcinoma the wall of the rectum loses 
its soft, velvety feeling and becomes dense and thick, but 
no obstruction and no ulceration can be appreciated (f). 
In examination for rectal carcinoma the patient should stand 
up and bear down, to bring the growth within reach. If 
nothing can then be felt, examination under an anaesthetic 
is indicated. 

Prognosis and Treatment.—An early diagnosis should be 
made if possible. Neglected cases run a fatal course of from 
two to four years, but life may be prolonged by an early 
excision of the neoplasm, as by Kraske’s operation. In 
some cases a radical cure has thus resulted. Lumbar colot- 
omy with the formation of an artificial anus may be indi¬ 
cated to relieve the constipation and to modify the pain. 

Cancer of the Caput Coli. 

The symptoms of cancer of the caput coli begin gradu¬ 
ally and are at first obscure. There is a gradual loss of flesh 
and strength, with varied digestive disturbances. In other 
cases pain is the first symptom noticed. The pain may be 
dull and boring or sharp and colicky. If there be obstruc¬ 
tion, pain is increased and symptoms of intestinal obstruc¬ 
tion gradually appear. Physical examination reveals a tumor 
in the caecal region—a tumor hard and irregular, either 
globular in shape or ovoid, its long axis agreeing with the 
course of the ascending colon. The tumor, which is usually 
adherent to the posterior abdominal wall, so that it is not 
apt to be movable, is most liable to be mistaken for fecal 
impaction or for a chronic appendicitis. The patient be- 


INTESTINAL OBSTRUCTION. 


5^5 


comes cachectic, loses flesh and strength, suffers from diar¬ 
rhoea or constipation, and dies exhausted or from intestinal 
obstruction. 

Treatment of cancer of the caput coli is merely palliative 
in cases in which the diagnosis is made too late to allow of 
resection of the intestine. 

Cancer of the Duodenum. 

Cancer of the duodenum usually presents itself as a mova¬ 
ble tumor which cannot be differentiated from malignant 
growths of the pylorus. The tumor may be displaced into 
the lower abdominal region by reason of the weight. Dila¬ 
tation of the stomach usually results, and the pancreatic 
duct and the bile-ducts may be obstructed. 

The treatment is palliative. 

Non-cancerous Tumors of the Intestine. 

Non-cancerous growths are so rare that they possess only 
pathological interest. 

Mucous polypi may occur, especially in children and in 
the rectum; or there maybe found pediculated fibromata. 
Lipoma, sarcoma, lymphangioma, and myoma have been 
described. 


INTESTINAL OBSTRUCTION. 

Etiology and Pathology. — 1. Internal strangulation , or 
“ internal hernia,” is the cause in one-third of the cases, and 
is the most frequent cause of obstruction in adults; 70 per 
cent, of the cases occur in males. The strangulation may be 
produced in various ways : A loop of intestine may be con¬ 
stricted by passing between peritoneal adhesions or by 
passing through apertures in the mesentery or the omen¬ 
tum, through the foramen of Winslow, or even through the 
diaphragm. Should the tip of Meckel’s diverticulum be 


526 MANUAL OF THE PRACTICE OF MEDICINE . 

adherent to the mesentery or to the abdominal wall, a ring 
will be formed, through which a coil of intestine may pass. 
In 90 per cent, of all cases the ileum is the portion of the 
intestine involved. Strangulation results in obstruction, 
ulceration, sloughing, and eventually in perforation. 

2. Intussusception , or invagination, which occurs in one- 
third the cases, is the most frequent cause of obstruction in 
children, one-third of the cases occurring during the first 
year, and one-half of the cases before the tenth year. This 
condition arises whenever one portion of the intestine slips 
into an adjoining part as a tuck may be taken in the finger 
of a glove; it appears to be due to irregular peristalsis, the 
receiving layer being drawn up by contraction of the lon¬ 
gitudinal fibres. In each intussusception three layers of 
intestine are brought in apposition : an outermost or re¬ 
ceiving layer (the intussuscipiens), the middle or returning 
layer, and the inner or entering layer. The outer and mid¬ 
dle layers are in contact by their mucous surfaces, the 
middle and the inner by their serous surfaces. There is 
thus formed a longitudinal tumor varying in length from 
several inches to as many feet, and the invagination extends 
at the expense of the outer layer. 

The intussusception is invariably downward. The affected 
parts become swollen, congested, and perhaps ecchymotic. 
In recent cases the peritoneum is merely congested and the 
intussusception may readily be reduced, but in cases living 
for two or three days the peritoneal surfaces become so agglu¬ 
tinated by fibrinous adhesions that reduction is no longer 
possible. The invaginated portion may slough and be passed 
by the rectum, so that spontaneous cure may result. Three- 
fourths of the cases of intussusception are of the ileo-caecal 
variety, in which the valve slips into the large intestine, gradu¬ 
ally inverting, appearing at the rectum in extreme cases. In¬ 
tussusception of the ileo-caecal variety or confined to the large 


INTESTINAL OBSTRUCTION. 527 

intestine may last in rare instances for months without giving 
rise to acute symptoms. 

3. Volvulus , or twist of the intestine, is the cause of the 
obstruction in one-seventh of the cases. Two-thirds of the 
cases of volvulus occur in men, and the condition is most 
frequent between the ages of thirty and forty. The twist, 
which is usually in the long axis of the intestine, is favored 
by a long mesentery, but one loop may be twisted around 
another or may be bent sharply upon itself. In one-half the 
cases the volvulus occurs in the sigmoid flexure, next fre¬ 
quently in the csecal region. The twisting interferes with 
the circulation of blood and leads to necrosis of the affected 
portion of the intestine. 

4. Acute obstruction from strictures and tumors may 
occur, but the obstruction is more apt to be chronic and 
progressive, although never complete. Narrowing of the 
lumen of the intestine may be due to the following condi¬ 
tions : ( a ) Congenital stricture as the result of fatal peri¬ 
tonitis, in which case the obstruction is usually in the 
rectum or the lower ileum ; or there may be congenital 
malformation resulting in imperforate anus or rectum. (&) 
Cicatricial stenosis may result from previous ulceration. 
(c) New growths of the intestine, especially epithelioma, (d) 
Compression of the intestine by abdominal or pelvic tumors. 
(c) Contraction of inflammatory exudate, especially with 
tubercular peritonitis. 

5. Obstruction may be due to foreign bodies within the 
intestine. Gall-stones may enter the intestine through the 
duct, or there may have been a communication between the 
intestine and the gall-bladder. Enteroliths may be formed 
by the phosphates of lime and magnesia being deposited 
about a central nucleus ; or the foreign body may be a 
tangled mass of worms. Fecal accumulation is a common 
cause of obstruction, and will elsewhere be described. 


528 MANUAL OF THE PRACTICE OF MEDICINE. 

Symptoms— The three cardinal symptoms are pain, 
vomiting, and constipation. The pain may begin suddenly, 
while the patient is in apparently good health, and is usually 
localized, intermittent, and colicky. It soon becomes more 
intense and continuous, and spreads over the abdomen, being, 
however, more severe in its original situation. Tenesmus oc¬ 
curs only if the rectum be involved. Vomiting is constant 
and distressing. The vomited matters are at first gastric, then 
bilious, and finally stercoraceous. The higher up the obstruc¬ 
tion the earlier does the fecal vomiting occur; but true fecal 
vomiting" cannot occur with obstructions above the upper 
third of the ileum. The vomiting may cease at the approach 
of the fatal issue, or it may be replaced by distressing and 
obstinate hiccough. Constipation is usually preceded by the 
emptying of the intestine below the seat of obstruction. 
There is also an absence of flatus. In intussusception there 
may be discharges of mucus and blood. If the obstruction 
be low down in the intestinal tract, the abdomen is greatly 
distended and active peristalsis is visible, but if the obstruc¬ 
tion be higher up these symptoms are not present. At first 
the abdomen is insensitive; later, exquisite tenderness is 
developed. The face becomes pallid and anxious ; there is 
incessant thirst; the pulse is feeble and either rapid or slow; 
the urine is diminished or suppressed. There is not apt to 
be fever; on the contrary, the temperature may be subnor¬ 
mal. Symptoms of collapse or of peritonitis appear, and 
the patient rarely lives beyond the fourth or the sixth day. 

Diagnosis. —The determination of the seat of the lesion 
is often extremely difficult. If the obstruction be in the 
duodenum or the jejunum, vomiting occurs early, collapse 
is rapid, there is no tympanites, and the urine is usually 
suppressed. If the lower ileum or caecum be obstructed, 
the abdomen is distended in the umbilical region, the flanks 
are flattened, and active peristalsis can be seen. If the 


1 NTES TINA L OBSTRUC TION. 


529 


colon or the rectum be occluded, the flanks become likewise 
distended, there may be tenesmus, and the symptoms are 
not as severe as in the preceding forms. If four quarts of 
water can be injected slowly so as to fill the colon and the 
caecum, the obstruction must be in the small intestine. 

Diagnosis of the Course of the Obstruction.—Intussusception 
is essentially a disease of children. A sausage-shaped 
tumor usually occurs before the third day in the region of 
the ascending or transverse colon. There is usually tenes¬ 
mus, with the passage of bloody mucus. Examination by 
rectum may reveal the lesion. Fecal vomiting is not com¬ 
mon, and abdominal distention occurs in only one-third of 
the cases. 

Strangulation is not common except during adult life. 
There is usually a history pointing to the presence of peri¬ 
toneal adhesions. Pain is excessive; vomiting is incessant 
and soon becomes fecal; prostration rapidly becomes ex¬ 
treme. There is absolute constipation, but no tenesmus, 
and there is no tumor to be detected. 

Volvulus is diagnosed with great difficulty, although it 
may be suspected if the sigmoid flexure be involved. As 
twists of the sigmoid flexure are often produced by the 
weight of accumulated feces, a history of fecal accumulation 
often precedes the accident. 

Foreign bodies usually lodge at the ileo-c?ecal valve. 
There may be the history of some bulky object swallowed, 
or of the passage of previous gall-stones. 

For the diagnosis of fecal impaction see pp. 534, 535. 

The diagnosis should also be made from functional 
obstruction occurring in hysterical patients, and usually 
following blows upon the abdomen, peritonitis, or the 
reduction of a hernia. The lesion seems to be a tempo¬ 
rary cessation of peristaltic movements, as the result of 
which the downward advance of the intestinal contents is 


34 


530 MANUAL OF THE PRACTICE OF MEDICINE. 

checked. In every case external strangulation by hernia 
must be excluded by careful search. Acute hemorrhagic 
pancreatitis may so closely resemble intestinal obstruction 
that a differential diagnosis cannot always be made. 

The prognosis of every case of obstruction is grave, and 
usually is absolutely unfavorable unless the obstruction be 
relieved by surgical measures. Spontaneous cure of intus¬ 
susception has been mentioned, but few children live long 
enough for the result to take place. Spontaneous cure may 
result in exceptional cases of strangulation by the formation 
of a fistula between two coils of intestine. 

Treatment should be prompt and energetic. Purgatives 
are absolutely contraindicated. The patient should be put 
under the influence of opium almost to the point of semi¬ 
narcotization, the respirations being kept between 10 and 
14 by its repeated administration. By this treatment all 
peristaltic action is checked, so that the gut will have a 
chance to untwist or to free itself from obstructing bands or 
from its invagination. The vomiting and pain are also 
checked, and the danger of collapse is lessened. 

Washing out of the stomach with warm water may 
be repeated three or four times a day. In some cases 
this treatment has been useful in diminishing peristalsis 
and in lessening the abdominal pressure above the ob¬ 
struction. The colon should be flooded with warm water, 
the patient being in the knee-chest position and preferably 
under the influence of an anaesthetic. Inflation of air may 
be practised, the air being introduced by a Davidson syringe, 
or the rectal tube may be attached to a siphon of carbonated 
water. These latter methods are most useful in cases of 
intussusception, but they are not devoid of danger, as rup¬ 
ture of the bowel has resulted when undue force has been 
used. Inflation and injection of water are of no service 
should the intussusception last longer than forty-eight 


hemorrhage from the intestine. 


53 1 

hours, as by that time inflammatory fixation will have 
occurred. 

These medicinal measures should not be continued after 
forty-eight hours, nor in any case in which the symptoms 
are rapidly becoming urgent, but laparotomy should be 
performed at once. Laparotomy should be done as early 
as possible in cases of strangulation, volvulus, and impaction 
of foreign bodies, before the interference with the circulation 
has led to sloughing of the intestinal wall. 

HEMORRHAGE FROM THE INTESTINE; 
ENTERORRHAGIA. 

Etiology. —Hemorrhage from the stomach is a symptom 
that may be produced in a variety of ways : 

1. By ulceration of the intestines of any form. 

2. By irritant and corrosive drugs. 

3. By local injuries, such as those inflicted by foreign 
bodies, by hardened fecal masses, and by intestinal parasites, 
especially by the anchylostoma duodenale and the distomum 
haematobium. 

4. By active congestion in severe inflammations, in intus¬ 
susception and volvulus, and following the reposition of an 
incarcerated hernia. 

5. By passive congestion with disease of the heart and 
lungs, with obstruction in the portal circulation and with 
hemorrhoids and venous varices. 

6. By diseases of the blood-vessels, especially amyloid 
degeneration, or by aneurysm or embolism of a branch of 
the mesenteric artery. 

7. By tumors of the intestine, especially cancer and polypi. 

8. By causes without the intestine, as when blood enters 
the intestine from the stomach or from a ruptured aneurysm 
of the abdominal aorta. 

9. By constitutional diseases, especially pernicious anae- 


532 MANUAL OF THE PRACTICE OF MEDICINE. 

mia, leukaemia, pseudo-leukaemia, scurvy, purpura haemor- 
rhagica, septicaemia, profound jaundice, yellow fever, acute 
yellow atrophy of the liver, and poisoning by phosphorus. 
Hemorrhage may also occur in conditions of hunger and 
inanition. 

io. Hemorrhages in the new-born (melaena neonatorum) 
may be due to acute fatty degeneration or to syphilitic 
degeneration of the blood-vessels, to haemophilia, or to 
puerperal infection. 

Symptoms.—The blood may be vomited or be passed 
by the bowel, or the patient may die before the blood ap¬ 
pears (concealed hemorrhage). Blood from the rectum or 
the sigmoid flexure is bright red, and its passage is accom¬ 
panied by straining. Blood from the lower bowel is also 
smeared over the fecal masses. Blood from the ileum is 
usually dark red, the normal color generally being restored 
by adding water to the stools, and its passage is accompanied 
by increased peristalsis and diarrhoea. Blood from the jeju¬ 
num and the duodenum is dark and tarry from the change 
of the haemoglobin into haematin. These dark stools may 
resemble those produced by eating huckleberries or by 
taking iron or bismuth, but the differential diagnosis is to 
be made positively by the spectroscope and by the finding 
of haematin-crystals in the stools. 

The general symptoms are those of hemorrhage in gen¬ 
eral. Following the hemorrhage the bowels may be obsti¬ 
nately constipated and there may be a high temperature 
(septic fever or resorption-fever). 

Treatment.—Absolute bodily and mental rest must be 
enforced, and no food should be allowed for from twenty- 
four to forty-eight hours. Opium should be given in doses 
sufficient to check peristalsis; this drug is also of service 
in controlling restlessness and collapse-symptoms. Ice 
applied to the abdomen, so often recommended, is not only 


FECAL ACCUMULATION. 


533 


useless but actually harmful, tending, as it does, to stir up 
peristaltic action. For large hemorrhages astringent drugs 
by the mouth do no good, but in repeated small hemorrhages 
ergotin, turpentine, erigeron, hydrastis canadensis, acetate 
of lead, gallic acid, and large doses of bismuth subnitrate 
are of great service. If the bleeding come from the rectum 
or low down in the colon, astringent injections may be em¬ 
ployed, but they should not be resorted to as a routine 
measure, because of their tendency to quicken peristalsis. 
Tamponage of the rectum causes retention of gas, straining 
efforts, and increased intestinal peristalsis, and it should not 
be employed except in cases of bleeding from the lower 
portion of the rectum. 

FECAL ACCUMULATION. 

Etiology.—Fecal accumulation may be primary, or sec¬ 
ondary to stricture of the intestine. In the primary cases 
there is usually the history of previous constipation, although 
at the time of examination the bowels may be loose. In 
other cases the accumulation results from weakness of ex¬ 
pulsive efforts, and is common after prolonged illnesses, as 
typhoid fever. 

Pathology.—The situation of the impaction is usually in 
the caecum or in the rectum, but it may be at any part of 
the large intestine. The fecal masses may totally occlude 
the lumen of the gut, or they may be packed in the lateral 
pouches of the colon, leaving a passage through which nor¬ 
mal stools may pass. If the accumulation be large, a tumor 
will be formed, which may give rise to pressure-symptoms, 
especially if the rectum be the seat of the impaction. The 
longer the fecal masses are retained, the harder they become, 
so that they may even resist the edge of a knife. The 
accumulation varies in amount, in extreme cases exceed¬ 
ing fifteen or twenty pounds in weight. 


534 manual of the practice of medicine. 

Symptoms.—Two distinct types of fecal accumulation are 
observed—a complete and an incomplete form. 

Complete Fecal Impaction. —( d ) If the ccecum be the 
seat of impaction, the patient will suffer from the effects of 
constipation and will complain of pain and tenderness in the 
caecal region. To these cases the term “ stercoral typhlitis ” 
is often applied. Examination will reveal the presence of a 
tumor—not soft, baggy, painless, and sausage-shaped, as 
ordinarily described, but hard, irregular, and more or less 
tender, so closely resembling the characteristics of a morbid 
growth that a diagnosis is impossible by examination alone. 
At some particular time the obstruction becomes complete. 
Constipation is absolute, not even gas being passed; the 
temperature rises to from ioi° to 104° F.; the pulse is 
rapid and feeble. The abdomen becomes tender and tym¬ 
panitic, and there is pain, either paroxysmal and colicky or 
like the exquisite pain of peritonitis. Respirations are rapid 
and thoracic. The case closely resembles one of appen¬ 
dicitis with general peritonitis, but in fecal impaction exam¬ 
ination reveals a greatly increased peristalsis of the intestine, 
whereas in peritonitis all peristaltic action is checked. Un¬ 
less relieved, gastric, bilious, and stercoraceous vomiting 
occurs; the patient is more and more prostrated, and dies 
with all the symptoms of intestinal obstruction. 

The prognosis of this form of impaction is good if the case 
be properly treated. Relapses, however, are likely to occur. 

Treatment .—In this form of impaction purgatives are 
absolutely contraindicated, as by the violent expulsive efforts 
of the bowel produced by their action the hardened mass is 
jammed more tightly into the distended intestine. Exactly 
the opposite treatment is indicated : opium is to be given in 
doses sufficient to check peristalsis and to relax the intes¬ 
tinal spasm at the seat of the impaction. Under this treat¬ 
ment the tumor can be felt to move along the colon from 


FECAL ACCUMULATION. 


535 


day to day. When the mass reaches the transverse colon, 
copious salt-water irrigations will bring away large quan¬ 
tities of hardened feces. When the impaction is once 
broken up opium should be discontinued and the use of 
laxatives should be begun, the best of these being castor oil 
in small repeated doses. Faradism and massage applied 
along the course of the colon are often of service in pro¬ 
moting the passage of the fecal masses. To prevent reac¬ 
cumulation, strychnine must be given for months to coun¬ 
teract the enfeeblement of the intestinal wall, and the bowels 
should be kept freely open by appropriate medication. 

(&) If the rectum be the seat of the impaction, there will 
result ineffectual attempts at defecation, with straining and 
tenesmus, so that fecal impaction should be suspected in 
every person, especially the aged and those who are con¬ 
valescing from a long, weakening illness, in whom the 
symptoms of dysentery appear. Pressure on the uterus 
may cause uterine symptoms. There may develop neuralgia 
from pressure on the sacral nerves, seminal emissions, or 
nocturnal enuresis. 

The diagnosis is readily made by rectal examination, 
which reveals the presence of hard scybalae in the rectum. 

Treatment consist in breaking the impaction mechan¬ 
ically and in removing the scybalae by the fingers, by the 
handle of a spoon, or by repeated enemata. 

Incomplete Fecal Impaction. —This form of impaction 
is usually seen in elderly persons with atony of the colon. 
The fecal masses are packed in the lateral pouches of the 
colon, leaving a passage channelled through the centre. 
The prominent symptom is diarrhoea, the loose stools aris¬ 
ing from the irritation of the large intestine above the im- 
paction. Some patients become poisoned by the accumu¬ 
lation, run down, and become so prostrated that the case 
may actually resemble typhoid fever. The condition is to 


536 MANUAL OF THE PRACTICE OF MEDICINE. 

be suspected in every case of chronic diarrhoea in old people. 
Examination may reveal scybalse in the rectum, or there 
may be a sense of resistance with some dulness over the 
descending colon. 

Treatment consists of purgation and colon-irrigation to 
bring away the fecal masses. Checking the diarrhoea with 
astringents regularly aggravates the condition. 

AMYLOID DEGENERATION OF THE INTESTINE. 

Etiology.—Amyloid degeneration of the intestine occurs 
as a secondary change in phthisis, in prolonged suppura¬ 
tion, especially of the bones, and in constitutional syphilis. 

Pathology.—The lesion involves the large and the small 
intestine and is especially marked in the lower ileum. The 
amyloid degeneration begins first in the walls of the 
smaller arteries, and in advanced cases may involve the 
whole thickness of the intestinal wall. Ulceration of the 
mucous membrane is not uncommon. 

Symptoms.—The principal symptom is a chronic diar¬ 
rhoea without fever (unless from the primary disease), pain, 
or tenderness. Blood and pus, if appearing in the stools, 
are indicative of ulcerations. The diagnosis is aided by the 
presence of the causative disease and by the finding of amy¬ 
loid changes in other organs, as the liver and the spleen. 


4. DISEASES OF THE PERITONEUM. 
ACUTE PERITONITIS. 

Etiology.—Peritonitis may be primary or secondary. 

1. Primary or idiopathic peritonitis is exceedingly rare. 
It may develop after exposure to wet and cold, or as a 
terminal event in Bright’s disease. 



ACUTE PERITONITIS. 


537 


2. Secondary peritonitis follows infection from inflamma¬ 
tion or perforation of any of the organs covered with peri¬ 
toneum. It thus may follow— (a) Penetrating wounds and 
laparotomies. (&) Rupture or perforation of any of the 
abdominal viscera, (c) Rupture of an abdominal abscess, 
such as appendicitis or suppurating inflammation of the 
Fallopian tubes. It has also followed rupture of an appar¬ 
ently normal Graafian follicle or extra-uterine gestation. It 
has also occurred after perforation of the diaphragm in em¬ 
pyema. (d) Extension from inflammation or ulceration of 
the stomach or intestines, cancer or suppurative inflamma¬ 
tions of the spleen, liver, pancreas, and retroperitoneal tis¬ 
sues, or strangulated hernia. ( e) Pelvic conditions—septic 
uterine conditions, decomposing thrombi, etc. Infection 
may be carried, as in the case of gonorrhoea, through the 
Fallopian tubes without the tubes being involved. 

Bacteriology.—The bacterium coli commune is one of 
the most frequent micro-organisms found in the peritoneal 
exudate, and is met with especially in peritonitis due to 
intestinal perforation. Next in frequency are the pyogenic 
micrococci, the streptococcus being usually associated with 
puerperal peritonitis, while the staphylococcus pyogenes 
aureus or albus is usually found in cases following lapa¬ 
rotomy. The diplococcus pneumoniae and the gonococcus 
have been found; the amoeba coli may occur in the peri¬ 
tonitis accompanying amoebic dysentery. 

Varieties.—There are three distinct varieties of peritonitis: 
I. Acute peritoneal sepsis; 2. Acute diffuse peritonitis; 3. 
Acute circumscribed peritonitis. 

Acute Peritoneal Sepsis. 

In this form of sepsis, which is also termed “acute peri¬ 
toneal septicaemia” and “ perforative peritonitis,” we have a 
simultaneous and rapid infection of the whole peritonea 


538 MANUAL OF THE PRACTICE OF MEDICINE. 

cavity after perforation of the stomach or the intestines, 
after rupture of large abscesses, or after septic penetrating 
wounds or laparotomies. 

Pathology.—The peritoneum may appear normal, or 
may be injected and without its normal lustre. In the peri¬ 
toneal cavity is a small quantity of sticky, non-purulent 
effusion, consisting chiefly of micro-organisms. This exu¬ 
date may be found on the surfaces of the peritoneum, and 
cocci may be found in the lymph-spaces. Feces, contents 
of the stomach, or pus from a ruptured abscess may be 
present, according to the nature of the primary cause. If 
the patient live long enough, purulent inflammation follows 
and the lesions of acute diffuse peritonitis are found. 

The symptoms are due to shock and to toxaemia from 
rapid absorption of ptomaines. There is usually a sudden 
sharp pain in cases of rupture or perforation, the pain ceas¬ 
ing as the patient passes into the condition of shock. The 
pulse becomes rapid and feeble ; the breathing is rapid and 
shallow; the skin is cold and clammy. Slight cyanosis 
appears, and the patient is restless. The temperature at the 
onset falls, only to undergo a subsequent rise before death 
to 105° or 106 0 F. Death from toxaemia results in from 
twelve to fifteen hours in the majority of cases. In cases 
of milder infection the patient may survive long enough to 
develop the symptoms of diffuse peritonitis. 

Acute Diffuse Peritonitis. 

This form of sepsis, which is also termed “ acute general 
peritonitis,” “purulent,” “progressive,” “ progredient,” or 
“ exudative peritonitis,” occurs when a general infection is 
not severe or sudden enough to cause death from toxaemia, 
or when successive areas of the peritoneum become in turn 
affected. 

Pathology.—The intestines are inflated with gas and pro- 


ACUTE PERITONITIS . 


539 


trude through the post-mortem incision. The peritoneum 
is congested or pale and soggy in appearance, and is covered 
with fibrin or with fibrin and pus which render opposing 
peritoneal surfaces adherent. There is an exudation of serum 
in cases of mild infection, or of pus if the infection be more 
severe, the pus being thin and yellowish or thick and creamy 
or putrid. The amount of the exudate varies from half a 
liter to twenty or thirty liters. There may be admixed 
contents of stomach or of intestines in cases of perforation. 
Blood is not found except after penetrating wounds or 
laparotomies. 

If the patient recover, the serum is absorbed, the fibrin 
and pus undergo emulsification and absorption, and the 
exudate becomes organized, so that the peritoneum becomes 
thickened and adherent. These connective-tissue adhesions 
interfere with peristalsis and may lead to internal strangu¬ 
lation. 

Symptoms.— Tympanites is usually marked; it is due to 
the paralytic condition of the intestine. The inflation of the 
intestines may be so marked that the thoracic viscera are 
displaced upward, interfering with the breathing and the 
action of the heart. The abdomen in these cases is usually 
protuberant, but in some cases it is of natural size, although 
the abdominal wall is tense and hard. In other abdominal 
diseases, such as intestinal obstruction, tympanites is also 
present, but is associated with active peristalsis, whereas in 
peritonitis the association of tympanites with absence of peri¬ 
stalsis is distinctive. Over the distended abdomen a tym¬ 
panitic note is obtained by percussion. Tympany over the 
normal liver-area is suggestive of gas within the peritoneal 
cavity. 

Pain and tenderness are usually at first limited to the local¬ 
ity first inflamed, but later they become more general. The 
pain is very severe, with acute exacerbations. The patient 


540 MANUAL OF THE PRACTICE OF MEDICINE. 

lies motionless on the back, with the knees drawn up to 
relax the abdominal wall, and the breathing is rapid and 
thoracic. Restless movements of the arms are often in 
sharp contrast to the immobility of the body and the lower 
extremities. In progressive peritonitis fresh encapsulations 
of pus are marked by an extension of the pain, and over 
these freshly involved areas the note is dull on light percus¬ 
sion. It is important to examine the patient frequently and 
to remember the extent and location of these areas of dul- 
ness. In rare cases it is possible for peritonitis to exist 
without either pain or tenderness. 

Vomiting is a frequent symptom. In some cases the 
vomiting appears to be due to irritability of the stomach 
or the diaphragm, and is accompanied by the muscular 
efforts of vomiting. The vomited matters are composed of 
food and bile-stained mucus. In other cases there is a re¬ 
gurgitation of gas from the intestine into the stomach, so 
that, without muscular effort, the gas is raised with a brown¬ 
ish or bilious fluid. In other cases, as death approaches 
there occurs, without effort, a regurgitation of a brown fluid 
which may possess a fecal odor. This sign is of serious 
import. 

Constipation is the rule, and results from diminished peri¬ 
stalsis. In some cases, however, diarrhoea may exist from 
the transudation of serum into the cavity of the intestine. 
This diarrhoea is more common with circumscribed peri¬ 
tonitis, especially if it has lasted for some time. 

The temperature is usually raised and runs an irregular 
course bearing no direct relation to the severity of the dis¬ 
ease. As a rule, a high temperature indicates an extensive 
peritonitis, but a low temperature does not necessarily in¬ 
dicate a mild attack. The fever may rise to 102° or 
104° F., but in some cases there occurs a sudden fall in the 
temperature with the appearance of collapse-symptoms, indi- 


ACUTE PERITONITIS. 


541 


eating the intervention of an acute peritoneal sepsis. Death 
soon occurs in these cases, and the temperature may be 
high again at the time of the fatal issue. A steady rise in 
temperature usually indicates a spreading peritonitis. In 
some cases with encapsulated collections of pus the temper¬ 
ature may become markedly remittent. Absence of fever 
is noted as a rare exception, especially in peritonitis of such 
acuteness and intensity that the symptoms merge into those 
of acute peritoneal sepsis. 

The pulse is rapid and “ wiry,” being more rapid than can 
be accounted for by the fever. As a rule, the pulse gives 
reliable information as to the general condition of the 
patient. 

The appearance of the patient is characteristic. The face 
is drawn and pinched; the nose is sharp and cold. The 
tongue has a tendency to become brown and dry even if the 
fever be moderate. 

The intellect remains surprisingly clear even to the last, 
but there may appear periods of muttering delirium asso¬ 
ciated with the symptoms of the “ typhoid state.” 

The duration of the disease is usually between two and 
seven days. 

The prognosis is exceedingly grave. Spreading infection 
of the peritoneum may be recovered from after laparotomy 
and drainage; recovery without operation may follow cases 
of mild infection in which the effusion is chiefly fibrino- 
serous without much pus; but in all cases of diffuse peri¬ 
tonitis, however mild the inflammation may appear, a most 
guarded prognosis must be given. Cases of streptococcus 
infection usually die. 

Diagnosis.—The following conditions are most apt to be 
mistaken for acute peritonitis: 

1. Hysterical peritonitis . Here every symptom of peri¬ 
tonitis may be reproduced exactly, even the collapse, the 


542 MANUAL OF THE PRACTICE OF MEDICINE. 

tympanites, and the fever, but other hysterical manifesta¬ 
tions are usually present, the duration of the attack is longer, 
and there may be recurrences. 

2. Intestinal obstruction. Here the cause is usually pres¬ 
ent (fecal accumulation, intussusception, or malignant 
growth), the temperature is not usually elevated, the vomit¬ 
ing is often stercoraceous, and intestinal peristalsis is in¬ 
creased. 

3. Acute hemorrhagic pancreatitis may exactly simulate 
peritonitis, so that a diagnosis between the two conditions 
cannot be made. 

4. Ruptured tubal pregnancy gives a previous history of 
cramp-like pains and cessation of menstruation. 

5. Rupture of an abdominal aneurysm usually gives rise to 
rapid collapse and intense anaemic symptoms. 

Acute Circumscribed Peritonitis. 

Etiology and Pathology.—Acute circumscribed peri¬ 
tonitis, which occurs in cases in which adhesions are suffi¬ 
ciently resistant to limit the infection, is more apt to occur 
with infection in the lower abdominal zone. The most 
frequent cases occur from inflammation of the appendix or 
from puerperal or gonorrhoeal infection of the uterus and 
the Fallopian tubes. The rupture of an ulcer of the stomach 
may lead to a circumscribed peritonitis within the lesser 
peritoneal cavity. There may thus form beneath the dia¬ 
phragm a large air-containing abscess to which the name 
“ subphrenic pyo-pneumothorax ” has been applied. If the 
localized abscess be small, the pus may eventually be ab¬ 
sorbed, encapsulated, or calcified; extensive collections may 
burrow or perforate. Gradual infection of the peritoneal 
cavity results in progressive peritonitis, and acute peritoneal 
sepsis may result from the internal rupture of the abscess. 

Symptoms are local and general. Local symptoms con- 


ACUTE PERITONITIS . 


543 


sist of pain, tenderness, and the presence of an inflamma¬ 
tory tumor. General symptoms at first are those of an in¬ 
flammatory character—prostration and continuous fever. 
Later appear the septic symptoms of pus-absorption, irregu¬ 
lar fever, chills, cold sweatings, diarrhoea, emaciation, and 
delirium at night. Ultimately septicaemia develops, with 
the symptoms of the typhoid condition. 

The symptoms of the disease may at any time merge into 
those of acute peritoneal sepsis or of progressive peritonitis. 

Treatment of Peritonitis. 

Peritoneal Sepsis .—The treatment is that of surgical shock 
—by stimulation, external application of heat, and small 
doses of opium. If the patient’s condition justifies the risk, 
laparotomy may be performed, perforations closed, and the 
peritoneal cavity cleansed with warm sterilized boric-acid 
solution. 

Diffused Peritonitis .—Mild cases may be treated medicin¬ 
ally at the start, but it is advisable for a surgeon to be in 
constant consultation in the case, so as to be ready for sur¬ 
gical interference should the medical treatment be unsuc¬ 
cessful. The object of the medical treatment is to prevent 
intestinal peristalsis, so as to allow of the formation of adhe¬ 
sions to limit the infection. The drug par excellence is 
opium, and the amount in which it can be given is remark¬ 
able, as in peritonitis there exists a tolerance of the drug. 
Alonzo Clark’s method was to give such doses as would 
keep the patient semi-narcotized, repeated doses being given 
as soon as the respirations exceeded twelve to the minute. 
In ordinary cases from 4 to 8 grains daily sufficed, but as 
much as 420 grains have been given in a single day. It is 
said, however, that the same tolerance does not exist for 
hypodermic doses of morphine as when the drug is given by 
the mouth. It is not now considered necessary to employ 


544 MANUAL OF THE PRACTICE OF MEDICINE . 

such heroic doses, but only as much morphine is given as 
will suffice to keep the patient free from pain. Larger doses 
than x /z grain every two or three hours are rarely required. 
Morphine even in these doses should always be given 
hypodermically. 

Concentrated saline laxatives, however, may be given at 
the onset in cases following operations or septic conditions. 

Local applications are often of great comfort and of un¬ 
questionable utility. For the earlier stages cold ice-bags 
or the cold Leiter coil is serviceable, but after five or six 
days hot applications seem to be preferable. The tym¬ 
panites may be relieved by turpentine stupes or by the 
passage of a rectal tube. Lavage of the stomach may re¬ 
lieve the distention of the upper portion of the abdomen. 
Fitz recommends the frequent puncture of the distended 
bowel with a small hollow needle in extreme cases of me- 
teorism, stating that the danger of extravasation or of the 
escape of gas into the peritoneal cavity is comparatively slight. 

The use of saline purgatives has been recommended by 
Lawson Tait and decried by others. Certainly it would 
seem that the increased peristalsis would rupture fine lim¬ 
ited adhesions, and the general use of laxatives is to be 
deplored. No harm results from constipation in peritoneal 
cases. Rectal injections may, however, be given to relieve 
the large intestine. In all cases of spreading peritonitis 
with urgent symptoms, surgical treatment is the only one 
that affords the patient any hope. 1 here is more danger 
in waiting too long for operative interference than there 
is in operating too early in the disease, when surgical treat¬ 
ment may not be necessary. 

Acute circumscribed peritonitis calls for surgical treat¬ 
ment to open and drain the abscess. The operation may 
be deferred in many cases until the limiting adhesions have 
had time to become firm. 


CHRONIC PERITONITIS. 


545 


CHRONIC PERITONITIS. 

Etiology.—Chronic non-tubercular peritonitis may suc¬ 
ceed an acute attack or may be chronic from the first. The 
most frequent cause appears to be repeated tappings for the 
removal ot ascitic fluid; but the condition may occur with 
chionic diffuse nephritis or with long-continued abdominal 
or pelvic abscesses. I he disease is more common in alco¬ 
holic patients. In some cases no definite cause can be 
assigned, but many of the so-called “ idiopathic ” cases ulti¬ 
mately are proven to be tubercular. 

Pathology.—-The peritoneum is thickened by connective 
tissue, and opposing surfaces are matted and massed to¬ 
gether by firm, thick adhesions. In extreme cases the peri¬ 
toneum is between one-fourth and one-half inch in thickness. 
In places there are congested patches covered with recent 
deposits of fibrin. The omentum, which is usually much 
thickened, is rolled up to form a sausage-shaped tumor 
lying transversely across the abdomen. The capsule of the 
liver or of the spleen may be thickened, contracted, and the 
volume of these organs correspondingly reduced. The 
mesentery is thickened and contracted. There may be but 
little serum, so that the process is described as “ adhesive ” 
or “prolifer^ive peritonitis,” but in other cases (“ascitic peri¬ 
tonitis ”) there is a quantity of liquid exudation, either free or 
encapsulated by adhesions. The ascitic form seems to be espe¬ 
cially common in children. Chronic peritonitis may be dif¬ 
fused, or the process may be limited to a circumscribed area. 

Symptoms are general and local. 

General Symptoms .—There is a progressive loss of flesh 
and of strength by which the patient becomes finally re¬ 
duced to semi-invalidism. The temperature may at times 
be slightly elevated. 

Local Symptoms .—Pain in the abdomen is constant and 

35 


546 MANUAL OF THE PRACTICE OF MEDICINE. 

annoying rather than actually severe. There is usually 
considerable tenderness on palpation. Disturbances in 
digestion are almost constant. The bowels are usually con¬ 
stipated, although periods of diarrhoea may occur from time 
to time. Distortions and flexions of the intestines may re¬ 
sult in obstruction, or the common duct may be so twisted 
or compressed as to cause persistent jaundice. Acute ex¬ 
acerbations of the inflammation may occur, with moderate 
fever and a marked increase of the pain and tenderness. 

In children between two and ten years of age a chronic 
peritonitis which cannot be traced to any cause is not un¬ 
common. The ascites is considerable, but the symptoms 
are not extreme and recovery usually ensues. 

The results of a physical examination are not always uni¬ 
form, and depend upon the amount of the thickening and 
adhesions, the rolling up of the omentum, and the presence 
or absence of a serous exudate. If there be much thicken¬ 
ing with matting together of the adhesions, the abdomen 
yields a doughy resistance to palpation, totally unlike the 
soft feeling of a normal abdomen. The whole abdomen 
may even appear to be filled with a resistant nodular 
tumor. If the omentum be rolled up, it may be felt as an 
irregular mass lying across the abdomen, and may be mis¬ 
taken for the nodular edge of an enlarged liver. If there 
be free effusion, the abdomen will be distended, and dulness 
or flatness will be obtained over the dependent portions of 
the abdomen, as well as over the flanks in the dorsal decu¬ 
bitus, with a tympanitic note over the uppermost portions. 
By changing the position of the patient there is a relative 
change in the position of the percussion-notes. Fluctuation 
can readily be appreciated. Small encapsulated collections 
of fluid, surrounded by thickened and adherent intestines, 
may so closely resemble tumors that a differential diagnosis 
from cancerous peritonitis is not always possible. 


TUBERCULAR PERITONITIS. 


547 


The duration of the disease is months or years. 

For the diagnosis from tubercular and cancerous peri¬ 
tonitis, see the articles treating of these diseases. 

The prognosis is bad, the patients usually dying ema¬ 
ciated ; but in some cases the disease may cease progress¬ 
ing, or recovery may follow operative treatment. 

Treatment is properly surgical. Ascitic accumulations 
should be withdrawn by puncture of the abdominal wall. 
Laparotomy, with the breaking down of adhesions and the 
drainage of encapsulated serous effusions, is often of cura¬ 
tive value. Medicinal treatment is symptomatic. It is 
claimed that benefit is derived from abdominal inunctions 
of mercurial ointment. 

CHRONIC HEMORRHAGIC PERITONITIS. 

This rare condition is analogous to chronic internal 
pachymeningitis. The peritoneum is thickened by con¬ 
nective tissue, and on its free surface are wide, thin-walled 
blood-vessels. By successive hemorrhages fibrin is de¬ 
posited in layers, so that the thickening is increased. The 
process, which is usually circumscribed, is most frequent in 
the pelvic region. 

TUBERCULAR INFLAMMATIONS OF THE 

PERITONEUM. 

The following forms of tubercular inflammations of the 
peritoneum are described: i. Acute tuberculosis of the 
peritoneum; 2. Acute tubercular peritonitis; 3. Chronic 
tubercular peritonitis. 

Acute Tuberculosis of the Peritoneum. 

In this form of inflammation the peritoneum is studded 
with tubercles as one of the lesions of acute miliary tuber¬ 
culosis. The peritoneum is otherwise normal, and shows 


548 MANUAL OF THE PRACTICE OF MEDICINE. 

no coincident inflammatory change, although there may be 
an effusion of clear serum. 

The clinical symptoms are latent or obscure. Pain and 
tenderness are rarely observed. The abdomen may be 
distended and may present the evidences of a peritoneal 
effusion. 


Acute Tubercular Peritonitis. 

Etiology. —This condition is seldom primary, but ex¬ 
tension of the disease to the peritoneum usually takes place 
from the intestines, the lungs, the pleura, .the mesenteric 
glands, the Fallopian tubes, or the genito-urinary tract in 
either sex. 

Pathology. —There is a miliary tuberculosis accompanied 
by the ordinary products of inflammation. The peritoneum 
is studded with tubercular granules or plates. Elsewhere 
the membrane is congested and coated with fibrin or with 
fibrin and pus. There is usually an abundant effusion of 
either clear or turbid serum, occasionally hemorrhagic, 
rarely purulent. 

The symptoms usually begin abruptly. There are more 
or less severe abdominal pain and tenderness, with the other 
local symptoms of a general peritonitis. The temperature 
runs an irregular course varying between 101° and 105° F., 
and is usually higher at night, although there has been ob¬ 
served an “ inverse ” temperature with evening remissions. 
The pulse becomes increasingly rapid and feeble. There is 
a progressive loss of flesh and of strength. There may be 
diarrhoea or constipation, or these conditions may alternate 
with each other. The “ typhoid condition ” ultimately 
develops. 

Physical Examination. —The abdomen is distended and 
tympanitic. Fluctuation is detected in one-third of the 
cases, especially in the earlier stages of the disease. Irreg- 


TUBERCULAR PERITONITIS. 


549 

ular masses may be detected on palpation in protracted 
cases ; these masses may be due (i) to a thickened and 
rolled-up omentum, (2) to encapsulated exudation, (3) to 
tubercular mesenteric glands, or (4) to retracted and thick¬ 
ened intestinal coils. 

Diagnosis.—The symptoms are not equally prominent in 
all cases, but there is considerable variety in their relative pre¬ 
ponderance. It the general outweigh the local symptoms, 
the case may closely resemble one of typhoid fever. The 
diagnosis may be rendered even more definite by a rose- 
colored eruption over the abdomen, resembling typhoid spots, 
which occasionally appears in tubercular peritonitis. If the 
local symptoms are the more prominent, the case may be 
regarded as one of non-tubercular peritonitis; but the diag¬ 
nosis is to be made from the latter condition by the absence 
of a cause for non-tubercular infection, by the presence of 
tubercular disease elsewhere, especially in the organs enu¬ 
merated under the heading of Etiology , and by the more 
protracted course of the disease. 

The duration of the disease is from four to six weeks. 

The prognosis is exceedingly bad, but is not absolutely 
hopeless. 

Treatment should be surgical. The abdomen should be 
opened and drained. Operative treatment is more effectual 
in chronic cases, but in a few acute cases cure has resulted 
from such peritoneal drainage. Medical treatment is en¬ 
tirely symptomatic. 

Chronic Tubercular Peritonitis. 

Etiology.—The etiology of the chronic is the same as 
that of the acute form of tubercular peritonitis. 

Pathology.—Two types are recognized : 

1. Tubercular Ascites .—The peritoneum is thickened and 
is studded with fibrous or cheesy tubercles in granules or 


550 MANUAL OF THE PRACTICE OF MEDICINE. 

in larger masses. The omentum is thickened and rolled up, 
the mesentery is retracted. There are but few adhesions. 
There is, however, an abundant serous effusion, giving rise 
to the symptoms and physical signs of ascites. The effu¬ 
sion is usually serous, but in rare instances it may be hem¬ 
orrhagic or milky. 

2. Tubercular Peritonitis with Adhesions .—All the viscera 
are matted together in one boggy mass, either by connective- 
tissue thickening and adhesions or by soft gelatinous fibrin. 
Fluid effusion is usually scanty and may be encapsulated. 
The retraction of the omentum and the mesentery is the 
same as in chronic non-tubercular peritonitis. Throughout 
the thickened peritoneum are old tubercles and cheesy 
masses. Fibroid transformation of tubercle is more com¬ 
mon in the peritoneum than in any other locality of the 
body. 

The symptoms of the tubercular resemble those of the 
non-tubercular form. There are, however, tubercular lesions 
elsewhere that modify the clinical picture of the disease, 
and the course of the tubercular form is more severe and 
uncompromising than that of the non-tubercular form. 
Some cases run a latent or an insidious course, and are acci¬ 
dentally discovered at a laparotomy or at the post-mortem 
table. In these cases the peritonitis is more apt to be cir¬ 
cumscribed, and usually it is found in the pelvis, from infec¬ 
tion through the Fallopian tubes. 

Malignant disease of the peritoneum, as a rule, progresses 
more rapidly than tubercular peritonitis, and is secondary 
to malignant disease of some one of the abdominal organs 
that can readily be diagnosed. 

The prognosis is grave, but is not so hopeless as might 
be expected. The brilliant results following laparotomy 
and drainage have made a favorable prognosis the rule. 

Treatment. —It is claimed that from 70 to 80 per cent. 


CANCER OF THE PERITONEUM. 55 I 

of the cases operated on have been cured, but evidence is 
wanting that even the majority of these cases were actually 
tubercular. In some cases merely an exploratory laparotomy 
in which the abdomen has been opened, inspected, and 
sewed up again at once has been productive of good results. 

The medicinal treatment is essentially constitutional and 
symptomatic. 

CANCER OF THE PERITONEUM. 

Etiology.—Primary cancer of the peritoneum is exceed¬ 
ingly rare, although cases of primary colloid growths of 
large size have been described. Secondary growths occur 
in connection with malignant disease of any of the abdomi¬ 
nal viscera. The disease, which is more common in women 
than in men, occurs during advanced life. 

Pathology.—The peritoneum is studded with carcino¬ 
matous nodules of various sizes, the favorite seats for the 
deposits being the omentum and the mesentery, the perito¬ 
neum near the umbilicus, and Douglas’s fossa. The 
nodules may be small and discrete or larger and confluent, 
so that tumors of considerable size may form. Unaccom¬ 
panied by coincident peritonitis, the process is spoken of as 
“ carcinosis.” Usually, however, the peritoneum is the seat 
of a chronic inflammation; it is thickened, the omentum is 
rolled up, and the peritoneal cavity contains an effusion 
which may be serous, hemorrhagic, or milky from the fatty 
degeneration of the cancer-elements. In rare cases the 
effusion may become purulent. To this form of malignant 
deposits with associated inflammation the term “ cancerous 
peritonitis ” is given. The retroperitoneal and mesenteric 
glands are usually involved, and the inguinal glands may be 
enlarged. Perforation or fistulae may result from the ulcera¬ 
tion of the cancer-masses, and fatal hemorrhage may occur 
from ulceration within the bowel. 


552 MANUAL OF THE PRACTICE OF MEDICINE. 

Colloid carcinoma involves the peritoneum diffusely, 
converting it to a thick, gelatinous mass, often of enormous 
size. 

Symptoms. — I. There are symptoms due to the primary 
o-rowth. Cachexia is usually evident before the peritoneum 
becomes involved. 

2. Symptoms of chronic peritonitis are present. In 
manv cases ascites and progressive emaciation are the prin¬ 
cipal complaints. Fever is usually present, but its course is 
similar to that of tubercular peritonitis. Pain and tender¬ 
ness are usually more marked than with ordinary chronic 
peritonitis, but in rare instances the course of the disease 
is painless throughout. 

3. Severe hemorrhages may result from ulcerations with¬ 
in the intestinal walls, or rapidly spreading peritonitis from 
perforation may develop. Cachexia, waxy pallor, and 
weakness increase with the progress of the disease. 

Physical examination yields no distinctive signs by 
which a positive diagnosis may be made. It there be much 
effusion, the tumors may be so obscured that a diagnosis 
from chronic peritonitis is impossible. Usually, after tap¬ 
ping, multiple nodules may be felt, but these nodules may be 
mistaken for the encapsulated exudate of a chronic tubercu¬ 
lar peritonitis. According to Osier, multiple nodules, if 
large, indicate cancer, particularly in persons above middle 
life, whereas nodular tubercular peritonitis is more common 
in children. The rolled-up omentum may be appreciated as 
an irregular mass lying across the upper abdominal zone; it 
has, however, no diagnostic value, as the same condition 
occurs in chronic tubercular or non-tubercular peritonitis. 
Examination by the rectum or the vagina should be resorted 
to in doubtful cases, as Douglas’s fossa is frequently in¬ 
volved early in the course of the disease. Secondary 
nodules about the navel are highly suggestive of cancer. 


ASCITES . 


553 


The diagnosis will be confirmed if cancerous fragments 
be removed through the trocar at the time of tapping. 
A milky appearance of the fluid is suggestive, but is not 
absolutely diagnostic. 

The further diagnosis from tubercular peritonitis has 
been spoken of under the latter disease. 

If the growth be colloid , the results of physical examina¬ 
tion are altogether different. There are no nodules and no 
ascites. The abdomen is symmetrically enlarged, often 
reaching enormous proportions. On palpation the abdomen 
is apparently filled with a semi-solid mass. 

The prognosis is absolutely bad. As cancerous peri¬ 
tonitis usually complicates pre-existing visceral cancer, the 
duration of the disease is seldom more than a few months. 
Cases of primary growth run a longer course. 

Treatment is entirely symptomatic. The fluid may be 
relieved by tapping if it produce discomfort, but the ascites 
rapidly returns. Opium should be given in doses sufficient 
to quiet pain. 

ASCITES ; HYDROPERITONEUM ; ABDOMINAL 

DROPSY. 

Etiology. —A serous exudate within the peritoneal cavity 
is common in all forms of chronic peritonitis, whether 
simple, tubercular, or cancerous. The term “ ascites, how¬ 
ever, should more properly be limited to a serous transuda¬ 
tion from stasis, without inflammatory changes. The 
ascites may thus be due— (a) to obstruction of the portal 
vein, either in the terminal branches within the liver, as in 
cirrhosis of the liver, or in a larger trunk without the liver 
as from thrombus-formation, from external pressure by pro¬ 
liferative peritonitis, new growths, or abdominal aneur¬ 
ysms ; (b) to general venous congestion arising in the course 
of chronic heart disease, emphysema, or interstitial pneu- 


554 MANUAL OF THE PRACTICE OF MEDICINE. 

monia; (V) to hydrsemic blood-conditions, as in Bright’s 
disease or in advanced anaemia. 

The ascitic fluid is pale yellow, with occasionally a green¬ 
ish tinge, and is usually clear. The specific gravity varies 
between 1010 and 1015, although in cases due to cancer of 
the liver the gravity may be as high as 1023. The fluid 
contains albumin, has the chemical characteristics of blood- 
serum, and may form a delicate fibrinous clot on standing. 
Ascitic fluid may at times present a milky appearance. If 
this appearance be due to the admixture of chyle (“ chylous 
ascites ”), the fat is molecular; if due to layers of fat-globules, 
the name “ adipose ascites ” is often applied to the fluid. 

Chylous ascites is due to injury to the thoracic duct by 
perforation, rupture, or by the filaria sanguinis hominis, or 
to its thrombosis or obliteration. In adipose ascites the fat 
originates from the fatty degeneration of cells, usually the 
product of a cancerous or tubercular peritonitis. 

The symptoms of ascites are due to the mechanical 
weight and pressure of the transudation. 

In ascites due to portal obstruction the fluid accumulates 
within the peritoneal cavity, sinking into the most depend¬ 
ent portions, while the abdominal organs that contain air 
float upon the fluid as far as their peritoneal attachment will 
allow. The fluid is freely movable, occupying the most 
dependent portions of the abdomen with every change of 
position. If the fluid does not thus move freely, but 
changes its position slowly and incompletely or remains 
immovable, inflammatory exudation is indicated. Pressure 
upon the iliac veins will cause secondary oedema of the 
lower extremities. In ascites due to diseases of the heart 
and the lungs or to hydrsemic blood-conditions the abdom¬ 
inal effusion is but an added symptom of a general dropsi¬ 
cal condition, and is associated with oedema of the lower 
extremities, and usually with hydrothorax. 


ASCITES. 


555 


Physical Signs.—In the dorsal position the abdomen is 
flattened in the umbilical region and bulges in the flanks. 
In the upright position the lower abdominal region is alone 
prominent. In extreme distention the whole belly is 
rounded and the skin of the abdominal wall is tense, shin¬ 
ing, and may present pinkish striae as in pregnancy. The 
navel is usually protuberant. Enlarged anastomosing veins 
are usually seen coursing over the abdominal wall. 

Percussion gives dulness over the fluid and tympany 
over the overlying intestines. By changing the position of 
the patient the relative areas of these percussion-notes 
becomes correspondingly altered. Percussion is important 
in differentiating between the distention of ascites and that 
of extreme meteorism. In cases of moderate effusion dul¬ 
ness appears in the umbilical region when the patient 
assumes the knee-chest position. 

Fluctuation is obtained by the transmission of a wave 
from one side of the abdomen to the other by one hand 
being placed over one flank while the other flank is lightly 
tapped. In this way even a small amount of fluid maybe 
detected with great accuracy. The sign, however, may fail 
when there is great effusion under high pressure. In fat 
subjects a fluctuation-wave may run across the lax, flabby 
abdominal wall, but this superficial wave may be checked by 
pressing the ulnar edge of the hand firmly upon the linea 
alba. 

The prognosis of ascites is dependent upon its cause. 

The treatment is that of the primary cause. Stimulants 
should be given to sustain a failing circulation. Anaemic 
conditions require appropriate treatment. The fluid may be 
diminished by the free use of diuretics and cathartics, 
should the patient’s strength allow of such treatment. 

Eventually tapping becomes necessary for the comfort of 
the patient, although the operation may have to be repeated 


556 MANUAL OF THE PRACTICE OF MEDICINE. 


frequently, as the accumulation tends to recur. Care 
should be taken before tapping to exclude a distended blad¬ 
der. The skin having been scrupulously sterilized, the 
puncture should be made with a straight trocar, in the 
median line midway between the symphysis and the navel, 
provided that previous percussion has not revealed an intes¬ 
tinal coil lying directly under the site of puncture. When 
the fluid ceases to flow the trocar is to be withdrawn, the 
opening being closed by a suture over which is applied an 
antiseptic pad. A tight many-tailed bandage applied dur¬ 
ing the tapping will facilitate the flow, and after the trocar 
is withdrawn will yield support to the relaxed abdominal 
wall; this application should never be omitted. The 
dangers of tapping are syncope, perforation of the intestine, 
infection of the peritoneum with unclean instruments, and 
hemorrhage from puncture of an artery of the abdominal 
wall. 


5. DISEASES OF THE LIVER. 

FUNCTIONAL DISTURBANCES OF THE LIVER. 

To appreciate the various symptoms caused by functional 
disturbances of the liver it is necessary to consider the 
normal functions of the liver, and to see what symptoms 
will necessarily arise from the perversion of each function. 

1. From disturbed glycogenic function the bodily heat is 
lowered, so that the patient becomes susceptible to cold ; 
glucose may pass the liver unchanged and may appear in 
the urine (glycosuria). 

2. Destructive metamorphosis of albuminoid matter not 
being properly performed, uric acid and sub-oxidized urea 
compounds are retained in the body, giving rise to head¬ 
ache, vertigo, mental dulness, and despondency. Muscular 



FUNCTIONAL DISTURBANCES OF THE LIVER. 557 

or articular pains are common. The kidneys may become 
irritated by the uric acid and the oxalate of lime, and a 

chronic nephritis may develop. In some cases renal calculi 
result. 

3. Defects in the quantity or the quality of the bile allow 
of general malnutrition. Fats not being easily absorbed, the 
patient becomes thin. There are constipation and intestinal 
flatulence. 

4. From the failure of the liver to destroy the poisons 
arising in the normal processes of digestion (pepto- 
toxines), or the alkaloids of intestinal fermentation, these 
toxic products pass the liver unchanged, and a general 
toxaemia is the result. 

Btiolog-y. —Functional disturbance of the liver may be 
primary or secondary. 

Primary cases arise—(1) From errors in diet. The food 
may be too rich, too excessive, or too abundant in fatty and 
saccharine ingredients, or there may be an over-indulgence 
in malt liquors. (2) From want of exercise and from 
deficient oxidation-processes. 

Secondary cases arise—(1) From structural changes in 
the liver. (2) From disorders of gastric or intestinal diges¬ 
tion. (3) PTom disorders of the heart and the lungs, inter¬ 
fering with a proper circulation of blood within the liver 
and with oxidation-processes. (4) Some cases seem to be 
due to mild malarial poisoning. 

Symptoms. —Individual symptoms may be inferred from 
the consideration of the preceding paragraphs. Clinically 
the cases may be divided into two groups : 

1. The whole nutrition of the patient is below par; he 
looks anaemic and imperfectly nourished, and the com¬ 
plexion has a muddy, sallow tinge. The tongue is furred 
and flabby. The appetite is generally lost, especially dur¬ 
ing the earlier portions of the day. The bowels are con- 


558 MANUAL OF THE PRACTICE OF MEDICINE. 

stipated, the stools being dryish and clay-colored. There 
is a disagreeable taste in the mouth, especially in the morn¬ 
ing, variously described as “bitter” or “pappy.” The 
breath is usually offensive. Headaches are frequent; they 
may be so persistent and severe as to suggest organic disease 
of the brain. Attacks of “ sick headache ” incapacitate the 
patient from time to time. The mental condition is one of 
apathy, with periods of irritability and depression. The 
urine generally shows deposits of urates, of oxalate of lime, 
or of uric acid. These patients are commonly described as 
“ bilious.” 

2. Patients of the second group of cases do not become 
emaciated nor do they lose strength. The intestinal symp¬ 
toms are slight, but the cerebral symptoms are prominent 
and distressing. Vertigo is often so pronounced that the 
patient is afraid to leave the house alone. There is loss of 
memory, with failure of the mind to concentrate itself for 
any length of time. Headache is frequent and distressing. 
There are alternate pallor and flushing of the face, with a 
sense of throbbing fulness in the head. The urine may 
contain oxalate of lime, uric acid or the urates, or may be 
normal. In these cases the symptoms are due to the vaso¬ 
motor disturbances of the vessels of the brain, due to their 
irritation by toxic products of body-waste or of intestinal 
digestion. 

The prognosis depends largely upon the will-power of 
the patient to carry out the necessary treatment. 

Treatment.—Any dietetic error should be corrected. 
The food should be simple and wholesome, and fatty and 
starchy food should be reduced in quantity. Alcoholic 
stimulants should, in general, be interdicted. The most 
benefit is to be derived from active exercise in the open air 
to the point of moderate fatigue. The exercise, once 
begun, should be systematic, should be graded to suit the 


CIRCULATORY DISTURBANCES OF THE LIVER. 559 

individual strength of the patient, and should be of such 
nature as to afford pleasure and enjoyment. The drug- 
treatment consists chiefly in controlling dyspeptic condi¬ 
tions, in giving laxatives when required, and in the use of 
cholagogues. Of the latter, podophyllin, rhubarb, ipecac, 
magnesium sulphate, hydrochloric acid, and salicylic acid 
are the most serviceable. The modified rhubarb and soda 
mixture, while unpleasant to the taste, is of great value: 


P^. Pulv. rhei, 

g r - u; 

Sodii bicarb., 

gr. v; 

Pulv. ipecac., 

£ r - i; 

Tinct. nucis vomicae, 

Tflv; 

Aq. menth. pip., 

3j.—M. 

Sig. One teaspoonful three times 

daily, before meals. 

CIRCULATORY DISTURBANCES OP THE LIVER. 


Anaemia.—This condition, frequently found post-mortem, 
is not accompanied by any symptoms. 

Active congestion was formerly regarded as a more im¬ 
portant condition than at the present time. Physiological 
congestion occurs after a hearty meal. Acute congestion 
may occur with infectious diseases, especially malaria, 
typhoid fever, and dysentery. 

The symptoms are not characteristic. There may be slight 
enlargement of the liver with tenderness on palpation. 

Treatment is by active purgation. 

Passive congestion (Chronic congestion; Nutmeg liver). 
—This condition occurs whenever there is a mechanical 
obstruction to the outflow of blood from the liver, during 
the course of heart disease with a failing right ventricle, with 
diseases of the lungs interfering with the flow of blood 
from the right to the left heart, and with pressure on the 
vena cava by thoracic tumors. 


560 MANUAL OF THE PRACTICE OF MEDICINE. 

Pathology .—‘The central vein of each hepatic lobule is 
dilated, and the liver-cells in its neighborhood become pig¬ 
mented and atrophied. The cells at the periphery of the 
acinus become fatty. The mottling of the reddish-brown 
depressed centre and the yellowish periphery of each acinus 
gives rise to the term “ nutmeg ” liver. In long-continued 
cases connective tissue may be deposited in and between 
the lobules, starting usually from the central vein. In the 
earlier stages the liver is enlarged, but the longer the con¬ 
gestion lasts, the smaller and denser the liver tends to 
become. 

The symptoms are chiefly those of the primary lesion 
with the attending venous congestions. There may be 
added symptoms of a moderate degree of portal obstruction 
(see Cirrhosis of the Liver). Nausea, vomiting, and even 
vomiting of blood may occur, and slight jaundice may be 
evident in the conjunctive and in the urine. 

The treatment is that of the original disease. Depletion 
of blood from the liver is accomplished by vegetable or 
saline laxatives. An occasional mercurial purgation by cal¬ 
omel or by blue pill is recommended. 

DISEASES OF THE CAPSULE OF THE LIVER. 

Acute Perihepatitis. 

Etiology and Synonyms.—The cause of acute peri¬ 
hepatitis may be direct violence, but usually there is found 
perforation of an ulcer of the stomach or the duodenum, or 
infection or rupture of a neighboring abscess, especially of 
the liver, the gall-bladder, or the right kidney. Synonyms: 
Subphrenic abscess; Subphrenic pyo-pneumothorax. 

Pathology.—The peritoneum of the liver and of the 
corresponding surface of the diaphragm is congested and 
covered with fibrin and pus. Adhesions form, allowing of a 


DISEASES OE THE CAPSULE OF THE LIVER. 561 


circumscribed peritoneal abscess (subphrenic abscess). The 
pus may be yellowish-red in color, from the presence in it 
of bilirubin, and it may contain crystallized fatty acids. If 
the cause be a perforation of an ulcer of the stomach or of 
the duodenum, the pus may be mixed with air (subphrenic 
pyo-pneumothorax). 

The symptoms of acute perihepatitis are those of a local¬ 
ized peritonitis. There are pain and tenderness with the 
general symptoms of fever. In perforative cases the onset 
is abrupt and may be accompanied by shock. In general, 
the course of the disease is that of an empyema or an ab¬ 
scess of the liver. Drainage or evacuation of the pus may 
be followed by cicatricial contraction of the abscess-wall, so 
that compression may be produced upon the liver, the vena 
cava, the bile-duct, or the portal vein. 

The physical signs resemble those of empyema or of an 
abscess of the liver. The right hypochondrium is dis¬ 
tended and motionless. There may be a friction sound 
detected early in the disease. Later the friction disappears 
and is replaced by dulness or flatness and absence of voice 
and breathing. 

Subphrenic pyo-pneumothorax may give physical signs 
similar to those arising from a like condition above the 
diaphragm. 

The diagnosis of perihepatitis is readily made, should the 
aspirating-needle draw ochre-colored pus containing bili¬ 
rubin and fatty acids. The etiology of the condition also 
gives a clue to the correct diagnosis. 

Treatment is entirely surgical, consisting in opening and 
draining the abscess. 

Chronic Fibrinous Perihepatitis. 

Etiology.—This condition may follow acute perihepatitis 
or may be chronic from the start, as the result of a 
36 


562 MANUAL OF THE PRACTICE OF MEDICINE. 

chronic irritation of a neighboring inflammation or of long- 
continued pressure over the liver. 

Pathology.—The peritoneum covering the liver is thick¬ 
ened and is adherent in places to opposed surfaces. Shrink¬ 
age of the fibrous capsule may result in atrophy of the liver 
or in constriction of the veins or the ducts. 

Symptoms.—There are no characteristic symptoms. A 
friction rale may be heard over the liver during inspiration, 
but this sign is inconstant. 

The treatment is that of the causative disease. 

Syphilitic Perihepatitis. 

The various syphilitic lesions of the liver will be consid¬ 
ered under the heading of Syphilitic Diseases of the Liver. 

ACUTE PARENCHYMATOUS HEPATITIS. 

Synonyms.—Acute yellow atrophy ; Malignant jaundice. 

Etiology .—Secondary acute fatty degeneration of the 
liver may occur with many of the infectious diseases, in the 
latter stages of cirrhosis or of biliary retention, with yellow 
fever, and with phosphorus-poisoning. 

Primary cases are exceedingly rare. Individuals under 
thirty years of age are more frequently attacked, and 
women, especially during pregnancy, are especially liable 
to the disease. At times several cases occur in one family 
or in barracks, showing an epidemic tendency. The actual 
cause of the disease is unknown, although it is supposed to 
be due to an unknown bacterial infection. 

Pathology.—The liver is reduced from one-third to one- 
half in size, and its capsule is in folds and wrinkles. The 
organ is jaundiced or mottled yellow and red, the latter 
color representing the more advanced stages of the lesion, 
in which all fat has been absorbed from the liver-tissue. 
Microscopically are found extensive fatty degeneration and 


ACUTE PARENCHYMATOUS HEPATITIS. 563 

necrosis of the liver-cells, ending in their ultimate absorp¬ 
tion. Crystals of leucin, tyrosin, and bilirubin may be 
found, and in most cases there is seen a small-celled infiltra¬ 
tion of the stroma. The body-tissues are deeply jaundiced. 
The spleen is large and soft in about half the cases. The 
heart-muscle shows granular degeneration. There is acute 
degeneration of the kidney. There are numerous hemor¬ 
rhages throughout the body. 

Symptoms.—In the majority of cases there is a premoni¬ 
tory gastro-duodenitis, with nausea, vomiting, and jaundice. 
The onset of the disease itself comes suddenly and severely. 

Nervous Symptoms .—There is violent headache. Active 
delirium, amounting to mania, may be so marked as to 
require physical restraint. The attacks of delirium become 
less and less severe and alternate with periods of stupor 
until finally the patient passes into the typhoid condition, 
with low, muttering delirium and extreme prostration. 

Jaundice, if not developed during the preliminary period, 
now becomes noticeable. Its absence is rare. The sudden 
occurrence of jaundice with violent cerebral symptoms is 
suggestive of this disease. 

Hemorrhages occur in the subcutaneous and submucous 
tissues, from mucous surfaces, and into internal viscera. 
Pregnant women abort with violent post-partum bleeding. 

Urinary symptoms are somewhat characteristic. The 
urine is diminished, jaundiced, and contains albumin and 
casts. Urea is markedly diminished, and may be altogether 
absent in the latter stages, and in its place are found crystals 
of leucin and tyrosin. The former, occurring in the form 
of globules resembling fat, is seen only upon evaporation of 
the urine ; the latter, in the form of needles, occurs as a 
spontaneous deposit. Leucin and tyrosin are not, however, 
constantly present in the urine of this disease. 

General symptoms are not characteristic. The tempera- 



564 MANUAL OF THE PRACTICE OF MEDICINE. 

ture may be normal, subnormal, or slightly elevated. A 
high ante-mortem temperature, however, is almost always 
observed. Vomiting is usually a prominent symptom, and 
blood may be raised. The bowels are constipated; the 
stools are clay-colored or may consist of blood. The pulse 
becomes rapid and feeble, the typhoid condition becomes 
more profound, and the patient dies, usually within a week, 
although the case may be somewhat more protracted. 

Physical examination shows a rapid diminution in the 
size of the liver. As the flabby liver tends to drop back, 
there may finally be only a slight line of liver-dulness in 
the axillary region, and no dulness at all in front. If the 
disease attack a previously enlarged liver, the diminution 
will be less marked and the diagnosis will be more difficult. 
The liver is usually tender on palpation or percussion. The 
diagnosis is further aided by the presence of an enlarged 
spleen, by the jaundice, and by the hemorrhages. 

The diagnosis may be made positively upon the associa¬ 
tion of severe jaundice, cerebral symptoms, diminished size 
of the liver, and the presence of leucin and tyrosin in the 
urine. 

The case may be mistaken for one of phosphorus-poison¬ 
ing, but in the latter condition there is the history of poison¬ 
ing, the presence of phosphorus in the vomited matters, the 
onset is more sudden, gastro-intestinal symptoms are more 
marked, and leucin and tyrosin are absent from the urine. 

The latter stages of hypertrophic cirrhosis may resemble 
acute yellow atrophy, but the liver is enlarged and the 
course of the disease is essentially chronic. 

Conditions of profound jaundice with cerebral symptoms 
(cholsemia) may so closely resemble acute yellow atrophy 
that a differential diagnosis is very difficult. 

Prognosis.—The disease is invariably fatal. 

The treatment is symptomatic. 


ATROPHIC CIRRHOSIS. 


565 


CIRRHOSIS OF THE LIVER. 

Synonyms,—Chronic interstitial hepatitis; Fibrous cir¬ 
rhosis. 

Three forms of cirrhosis of the liver are recognized: 1. 
Atrophic cirrhosis; 2. Hypertrophic cirrhosis ; 3. Syphilitic 
cirrhosis. The “ Glissonian cirrhosis ” has been described 
under the heading of Chronic Perihepatitis. 

Atrophic Cirrhosis. 

Etiology.—Fibrous disease of the liver is almost regu¬ 
larly due to the action of irritants brought to the liver by 
the blood-vessels. In over two-thirds of the cases the im¬ 
mediate cause is alcohol, especially the stronger liquors. 
There may be the history of excessive indulgence, or the 
habit of “ nipping” may be confessed. In some cases indul¬ 
gence in the lighter wines or in malt liquors may lead to 
the disease. Other irritants entering the liver by the portal 
vein may be adduced as causes of the disease—highly-spiced 
food and the ptomaines and other alkaloids of intestinal 
digestion—but upon this point satisfactory evidence is lack¬ 
ing. Cirrhosis may follow rickets, scarlet fever, or typhoid 
fever, or may result from long-continued passive hypermmia 
of the liver. In coal-miners the disease may follow the 
swallowing of coal-dust, which is deposited as solid pigment 
in the liver. There has been described a senile form of 
cirrhosis analogous to other arterio-sclerotic changes in the 
different viscera. 

Cirrhosis of the liver is far more common in men than in 
women, because of their more frequent indulgence in alco¬ 
hol. It usually occurs between the ages of thirty-five and 
sixty years, and it is far less common in children than was 
formerly supposed, although in them the majority of cases 
are of syphilitic origin. It is a peculiar fact that cirrhosis 
is exceedingly rare in the negro, although in this race in- 



566 MANUAL OF THE PRACTICE OF MEDICINE. 

temperate habits are common. Two autopsies only of this 
disease have been made at the Colored Hospital in New 
York during the past twenty-five years. 

Pathology.—The liver is small, hard, and dense. Its 
weight may not exceed a pound or a pound and a half. 
The surface is granular, and the capsule is usually thick¬ 
ened. On section the organ may be bile-stained or may 
present grayish-white streaks of connective tissue. It was 
owing to the yellow appearance of the organ that the name 
“ cirrhosis ” (xiypoz, yellow) was first applied by Laennec. 
A primary increase of the size of the liver does not occur. 
Upon close examination the essential lesion is seen to con¬ 
sist of the formation of connective tissue within the liver, 
either loose and cellular or dense and fibrillated. The 
fibrous tissue usually extends about the radicles of the por¬ 
tal vein at the periphery of the acinus, giving the organ a 
finely granular appearance; or the connective tissue may 
surround groups of acini, resulting in a coarsely granular 
appearance. The tissue may extend into the liver from the 
capsule in large irregular streaks and bands, although this 
arrangement is more common in syphilitic cirrhosis. 

Pressure-changes are seen in the liver-cells, the blood¬ 
vessels, and the gall-ducts. The liver-cells, especially at the 
periphery of the acini, undergo fatty degeneration and 
become atrophied or flattened by pressure. 

The rootlets of the portal vein between the lobules are 
pressed upon and obliterated. This interference with the 
portal circulation gives rise to the important lesions of 
portal obstruction. There is usually an increase in the size 
of the hepatic artery furnishing blood to the new fibrous 
tissue. The gall-ducts may be the seat of a catarrhal 
inflammation or may become obliterated. In some cases 
there occurs an irregular production of new gall-ducts. 

Secondary lesions result directly from the portal obstruc- 


CIRRHOSIS OF THE LIVER. 


567 


tion. The spleen becomes congested and hyperplastic. 
I he stomach and the intestines are congested or show 
chronic catarrhal inflammation. Ascites results from the 
stasis, may reach an extreme degree, and may be accom¬ 
panied by a mild form of chronic peritonitis. Hemorrhoids 
result from congestion of the veins of the rectum. There 
are evidences of collateral circulation between the branches 
of the portal veins and those of the vena cava, at the junc¬ 
tion of the oesophagus and the stomach, along the sigmoid 
flexure and rectum, in the retroperitoneal plexus, and about 
the umbilicus. The radiating varicose veins about the latter 
situation have received the name of “ caput Medusae.” The 
branches of the internal mammary and epigastric veins also 
become dilated and tortuous. 

Associated lesions are not due directly to the cirrhosis, 
but are frequently found in the same patient, and arise from 
the same etiological factors as does the fibrous disease of 
the liver. These lesions comprise endocarditis, atheroma 
of the aorta, endarteritis, emphysema, and chronic diffuse 
nephritis. Acute tuberculosis is a not infrequent compli¬ 
cation. 

Symptoms.—There may be an antecedent alcoholic 
gastritis. When cirrhosis develops, the symptoms present 
themselves in four groups : 

1. Symptoms of functional disturbance of the liver. The 
various intestinal, urinary, cerebral, and nutritive symptoms 
are present as in the cases previously described, and cir¬ 
rhosis should be suspected if these symptoms occur in an 
alcoholic subject. 

2. Symptoms of obstructed portal circulation are more dis¬ 
tinctive. Gastro-intestinal symptoms are those of conges¬ 
tion or chronic inflammation, dyspepsia, vomiting, haema- 
temesis which may be profuse or even fatal, constipation, and 
haemorrhoids. Ascites gives rise to enlargement of the 


568 MANUAL OF THE PRACTICE OF MEDICINE . 

abdomen and to dyspnoea; the transudation may press 
upon the iliac veins, causing oedema of the lower extrem¬ 
ities. As long, however, as compensatory circulation is 
maintained, the obstructive symptoms are slight or absent. 

3. Symptoms of jaundice are due to the obliteration or 
catarrhal inflammation of the bile-ducts or to gastro¬ 
duodenal catarrh. The jaundice is rarely marked at first, 
amounting only to a muddy, sallow tinge. The facies is 
fairly characteristic: the skin is dry and of an icteroid hue; 
the nose and the cheeks show distended veins; the eyes 
are sunken and watery. From time to time attacks of 
more severe jaundice occur, and in some instances, espe¬ 
cially toward the termination of the disease, the jaundice 
becomes extreme and is accompanied by cerebral symp¬ 
toms. 

4. Symptoms of toxcemia may develop at any time. The 
patient may become actively delirious, noisy, and talkative; 
or he may become stupefied, with periods of semi-coma and 
muttering delirium, or may even develop convulsions. 
These symptoms may be due to intense jaundice, to alco¬ 
holism, or to uraemia, while in other cases the exact nature 
of the toxaemia cannot be ascertained. The course of the 
disease is usually afebrile throughout, except that a moder¬ 
ate temperature may occur as a terminal symptom. At no 
time is there pain or tenderness over the liver. 

Physical examination shows a diminution in the size of 
the liver, an enlargement of the spleen, and the presence of 
ascites and of anastomosing veins. A positive assurance 
that the liver is actually diminished in size is often lacking, 
as an apparent but not a real, diminution may be caused by 
the overlapping of the liver by an emphysematous lung, or 
by the liver being tilted upward by a distended stomach or 
colon ; or the lower line of liver-flatness may be obscured 
by tympany from intestinal distention. In other cases the 


CIRRHOSIS OF THE LIFER. 


569 

cirrhosis may occur in a liver previously enlarged by waxy 
or fatty change. The liver is thus rendered smaller than its 
previous size, but still may be larger than normal (see 
Hypertrophic Cirrhosis). The enlargement of the spleen 
is best determined by palpation, as the percussion-bound¬ 
aries may be obscured by tympanites, by the solid or liquid 
contents of the stomach or the colon, or by the ascites. It 
is important to remember that the spleen may not be in¬ 
creased in size if there be continued diarrhoea or vomiting - 
or if its capsule be thickened from perisplenitis. 

Prognosis.— Hie course of the disease is protracted. 
The exact duration of any given case cannot be determined 
accurately, as the onset is insidious. If the patient abstains 
from his alcoholic habit, the lesion may not develop further, 
so that he may live for years. In ordinary cases the end is 
reached within a year or two after the diagnosis is made. 
Death may result from haematemesis, from Bright’s disease, 
from delirium tremens, from the cerebral symptoms of 
severe jaundice, or from toxaemia and exhaustion. In the 
latter instance the patient becomes anaemic and emaciated, 
the enlarged ascitic abdomen being in marked contrast to 
the emaciated chest and extremities. Cerebral symptoms 
develop—stupor, muttering delirium, and semi-coma. The 
pulse becomes rapid and feeble, and death finally results. 

Treatment.—The patient should abstain from alcoholic 
drinks and from highly-seasoned food. The diet should be 
of the simplest character, and the value of a prolonged milk 
diet cannot be overestimated. Exercise should be moder¬ 
ate and gradual; the skin is to be kept active by baths and 
frictions; the bowels should be kept open; and all errors 
of digestion should receive appropriate treatment. In pa¬ 
tients with a syphilitic history mercury and potassium 
iodide may be given. Quinine and arsenic are indicated if 
the patient lives in a malarial locality. Cholagogues are 


570 MANUAL OF THE PRACTICE OF MEDICINE. 

indicated for the relief of the functional disturbances of the 
liver. When symptoms of portal obstruction appear, the 
indication for treatment is to deplete the engorged intestinal 
vessels by occasional catharsis. For this purpose from half 
an ounce to an ounce of magnesium sulphate may be given 
in a concentrated solution before breakfast, or any of the 
vegetable purges may be administered. An occasional dose 
of calomel or of blue pill is also of service. The ascites is 
to be relieved by diaphoretics, cathartics, and diuretics. 
Tapping should not be resorted to unless the ascites be 
distressing and be unrelieved by medicinal treatment, as the 
operation usually must be repeated frequently, and cerebral 
symptoms are apt to follow the withdrawal of the effusion. 
Repeated tappings, moreover, may result in chronic peri¬ 
tonitis. Toward the close of the disease alcohol may be 
necessary as a stimulant. 

Hypertrophic Cirrhosis. 

Of hypertrophic cirrhosis three forms are described : 

1. In the first variety the lesions are the same as in the 
atrophic form, but the increase of the connective tissue is 
greater than can be compensated for by the atrophy of the 
liver-parenchyma. The result is a cirrhotic liver of large 
size. The secondary lesions and the symptoms are identical 
with those of the atrophic form. 

2. Biliary cirrhosis , or hypertrophic cirrhosis with jaundice , 
usually results from chronic bile-retention, and frequently 
follows chronic obstruction of the common duct by a gall¬ 
stone, by cicatricial contraction, or by pressure from without. 
A primary form of biliary cirrhosis has been described. 
The bile-ducts become distended and are surrounded by 
new deposits of connective tissue. Fatty degeneration and 
atrophy of the liver-cells are not marked, the lesion differ- 
ing greatly in this regard from that of the atrophic form. 


CIRRHOSIS OF THE LI PER. 


571 


The liver is symmetrically enlarged, extending to the umbil¬ 
icus or even to the level of the anterior superior spines, is 
deeply jaundiced, and is resistant to the feeling and to the 
knife. Secondary lesions of portal obstruction are usually 
present, but to a less degree than in the atrophic form. 
Ascites is usually absent, although it may appear late in the 
disease. Jaundice is persistent and extreme throughout, 
yet the feces may be bile-stained. Hemorrhages in biliary 
cirrhosis are infrequent. At any time there may appear 
symptoms closely resembling those of acute yellow atrophy. 
The temperature rises to 102°, 104°, or even to 106° or 
108 0 F., jaundice rapidly becomes more extreme, delirium 
and convulsions appear, and a fatal issue rapidly follows. 
Leucin and tyrosin, however, do not appear in the urine. 
In other cases death results from emaciation and debility. 

The course of the disease is from three to seven years. 

The treatment is that of cirrhosis in general. Good re¬ 
sults have followed the frequent use of small doses of cal¬ 
omel, one grain being given several times a day for several 
days, and then discontinued should too free purgation fol¬ 
low or should stomatitis threaten, to be again administered 
after five or six days’ interval. 

3. Fatty Cirrhosis .—In this form of cirrhosis fatty and 
cirrhotic changes are found associated. The liver is large 
and resembles a fatty liver, but it is firmer, more resist¬ 
ant to the feeling and to the knife, and microscopically 
shows an increase in the connective tissue. The clinical 
course is that of atrophic cirrhosis, differing only in the fact 
that the liver is found to be enlarged. This form of cirrhosis 
is very common. 


Syphilitic Cirrhosis. 

Etiology.—Syphilitic disease of the liver may be the re¬ 
sult of hereditary syphilis, occurring as a congenital mani- 


572 MANUAL OF THE PRACTICE OF MEDICINE. 

festation or during childhood, or the liver may be affected 
as a tertiary lesion of the acquired disease. 

Pathology.—Pathologically, three types of syphilitic dis¬ 
ease of the liver may be described, but they are usually 
combined and blended with each other: 

1. Syphilitic Perihepatitis. —The capsule of the liver is 
thickened and is adherent to opposing peritoneal surfaces. 
From the thickened capsule bands of connective tissue pass 
into the substance of the liver, forming fibrous scars that 
cause considerable deformity. 

2. Diffuse Syphilitic Hepatitis. —The liver is large, firm, 
and resistant. Its color may be compared to that of sole- 
leather, or its appearance may resemble that of the amyloid 
liver. Microscopically the hepatitis does not present essen¬ 
tial differences from the lesion of ordinary cirrhosis, al¬ 
though in some instances large groups of acini are sur¬ 
rounded by fibrous bands visible to the naked eye, and 
extensive puckered cicatrices may be found. Gummata 
are usually present at some stage of the disease. The lesions 
of portal obstruction are regularly present. 

3. Gummata occur as nodules varying in size from that 
of a pea to that of a lemon. Fresh gummata are reddish- 
gray and of a translucent appearance. The older gummata 
show at their periphery a connective-tissue capsule; their 
centres may become cheesy, fibrous, or puriform, or they 
may be infiltrated with lime-salts. Smaller gummata un¬ 
dergo fibroid transformation and result in disfiguring cica¬ 
trices. Gummata alone cause neither portal obstruction 
nor jaundice, as a rule, unless they form in a locality where 
pressure on the portal vein or the bile-duct is possible. 

Symptoms.— 1. Of the Perihepatitis. —Pain and tender¬ 
ness are commonly observed; the movements of the liver 
during respiration are impeded ; and a friction sound can 
usually be detected by auscultation. 


ABSCESS OF THE LIVER. 


573 


2 . Of the Diffuse Hepatitis. —The symptoms resemble 
those of cirrhosis, but a primary enlargement of the liver 
may possibly occur. 

3 - Of Gummata .-—The symptoms are similar to those 
produced by multiple tumors. The gummata are usually 
situated near the suspensory ligament and on the under 
surface of the liver, so that an irregular lower border may be 
appreciated. Inequalities of the surface may be detected. 

The diagnosis of syphilitic disease of the liver is made by 
the consideration of the following points: i. The absence 
of alcoholic history. 2. The presence of congenital or the 
late forms of acquired syphilis. 3. The patient is frequently 
a young child. 4. The symptoms of cirrhosis are compli¬ 
cated by those of perihepatitis and of gummata. 5. The 
beneficial results of treatment. 

Treatment consists in the administration of potassium 
iodide in large doses, preferably combined with mercurials. 
If the treatment be prompt and vigorous, the results are 
often brilliant; but if the treatment be begun too late, cica¬ 
tricial bands and diffuse hepatitis may remain, for which 
further treatment is of no avail. In other respects the treat¬ 
ment of the case is that of ordinary cirrhosis. 

ABSCESS OP THE LIVER (SUPPURATIVE 

HEPATITIS). 

Etiolog’y.—Abscess of the liver is due to infection by 
micro-organisms capable of causing suppuration. Of these 
micro-organisms the pyogenic micrococci and the amoeba 
coli are the most important. The infecting germ may enter 
the liver by several channels : 

1. Through traumatism , by injuries, by foreign bodies, 
and by parasites. Suppurating hydatid cysts are not un¬ 
common. 

2. Through the portal vein. Liver-abscess thus compli- 


574 MANUAL OF THE PRACTICE OF MEDICINE. 

cates intestinal ulcerations (especially those of dysentery, 
in which the infective agent is the amoeba coli), abdominal 
abscesses, operations upon the rectum, and suppurative in¬ 
flammations of the portal vein itself. 

3. Through the umbilical vein in new-born children, fol¬ 
lowing infection of the navel. 

4. Through the hepatic artery in pyaemia, in malignant 
endocarditis, and in gangrene of the lung. 

5. Through the bile-duct. Infection through this channel 
is favored by the presence of cholangitis or of gall-stones. 

6. In some cases no cause can be ascribed for the infec¬ 
tion, and to these cases the names “ idiopathic ’ and “ tropi¬ 
cal ” abscess are given. This variety of abscess, which is 
most common in India, may occur in the Southern United 
States, but it is infrequent in Northern cities. The infecting 
aeent in most of these abscesses is the amoeba coli, although 

o 

the symptoms of dysentery may be absent. 

Abscess of the liver occurs with greatest frequency in 
men, and in those of adult years. 

Pathology. —The wall of the abscess is usually irregular 
and jagged ; it is composed of necrotic liver-tissue infiltrated 
with fibroid serum and pus, and the surrounding liver-tissue 
is hyperaemic. In protracted cases a connective-tissue cap¬ 
sule may be formed. The pus may be thick and creamy, 
or it may be thin, curdy, and of a reddish or brownish color, 
from pigment derived from blood-cells and broken-down 
liver-parenchyma, thus resembling anchovy sauce in appear¬ 
ance. In other cases the pus is yellowish-green or brick- 
red in color, from the staining of bile or of bilirubin-crystals. 
The pus, which is usually foul-smelling, is generally shown 
by bacterial examination to be sterile. There may be but 
one abscess, as in the tropical variety, or the abscesses may 
be multiple, as is the case with pyaemia and with suppura¬ 
tive inflammation of the portal vein or of the bile-passages. 


ABSCESS OF THE LIVER. 


575 


Single abscesses may reach the size of a cocoanut; multiple 
abscesses vary in size up to that of a walnut, but by their 
coalescence still larger abscess-cavities may be formed. 
Seven-tenths of all abscesses of the liver occur in the right 
lobe, usually toward the convexity. 

Abscesses in the liver evince a tendency to approach the 
sutface and to rupture. In 5 per cent, of all cases rupture 
into the peritoneal cavity occurs. Usually, however, the 
peritoneum is shut off by adhesions, so that the abscess 
ruptures into neighboring organs. Rupture upward into 
the right lung occurs in 9 per cent., into the right pleura in 
5 per cent., of all cases. Perforation of the pericardium or 
of the vena cava may occur. Rupture downward may occur 
into the liver, the intestine (3 per cent.), or the kidney. The 
abscess may approach the chest-wall or the abdominal wall 
or may open into the gall-bladder. In rare cases the abscess 
remains stationary. A connective-tissue capsule is ulti¬ 
mately formed, enclosing the purulent contents, which may 
become inspissated and cheesy. 

The symptoms are general and local. 

General symptoms indicate the presence of pus within the 
body. Chills are common at the onset, and may be re¬ 
peated throughout the disease. The chills may be erratic 
and may be followed by fluctuations in temperature and by 
cold sweating—a symptom-complex of pus-infection ; or 
the chills may be repeated in multiple abscesses whenever a 
new focus of suppuration forms. The fever is usually 
irregularly remittent, although in some cases the remissions 
are so periodic as to suggest malarial fever. In some cases, 
especially if long-protracted, fever may be entirely absent. 
Prostration is evident from the first; the pulse becomes 
rapid and feeble, and the patient finally passes into a typhoid 
condition. The appearance of the patient is somewhat 
characteristic. The skin is sallow and of a slightly jaundiced 


576 .MANUAL OF THE PRACTICE OF MEDICINE. 

hue, and the expression strongly suggests the existence of 
abscess. Marked jaundice is rare. The bowels may be 
constipated, or there may be diarrhoea. Amoebae coli may 
be found in the stools, giving a clue to the diagnosis. The 
general symptoms may be so complicated or masked by 
those of the primary disease that no special features may be 
added to the case. 

Local symptoms, due to localized suppuration, consist of 
pain and tenderness. The pain may be dull in case of a 
central abscess, or sharp and cutting if the peritoneum over 
the abscess become inflamed. In many cases the inflamma¬ 
tion extends from the peritoneum to involve the diaphrag¬ 
matic pleura, so that a true pleuritic pain occurs. Pain of a 
peculiarly heavy, dragging character usually develops when¬ 
ever the patient lies upon the left side. Tenderness 
becomes more marked when the peritoneum over the liver 
is involved. In deep-seated abscess there may only be 
some rigidity of the abdominal wall in the hypochondrium. 
In some cases pain and tenderness are slight or are alto¬ 
gether absent. 

Portal obstruction occurs only if the abscess happen to 
press upon the portal vein, but the symptoms are never 
extreme. 

A catarrhal inflammation of the bile-ducts with jaundice 
may or may not be present, but the jaundice rarely becomes 
marked. 

Physical Examination.—I. Of the Large Single Ab¬ 
scess .—The liver is tender on palpation and is irregularly 
enlarged. There may be appreciable bulging over the 
abscess, depending upon its size and its position. A large 
superficial abscess may give rise to fluctuation if the perito¬ 
neal surfaces over the abscess be adherent. As the 
abscess is usually in the right lobe near the convex 
surface, the area of liver-dulness rises in the axilla, fre- 


ABSCESS OF THE LIVER. 


5 77 

quently to the fifth rib, and extends across the back on a 
level with the angle of the scapula. In these cases an 
erroneous diagnosis of empyema is frequently made. Large 
abscesses of the upper surface of the right lobe, extending 
forward, may give rise to dulness as high as the second rib 
in front and the spine of the scapula behind, while the liver 
itself is displaced downward, the lower edge being fre¬ 
quently as low as the level of the umbilicus. Abscesses 
of the right lobe tend to point in the seventh and eighth 
spaces in the mammary line or below the costal arch. Ab¬ 
scesses of the left lobe usually point in the median line just 
below the ensiform cartilage 

2. Multiple Abscess of Pycemic Origin .—The liver is 
usually symmetrically enlarged and tender. Pointing, fluc¬ 
tuation, and bulging are not observed. 

In cases of doubtful diagnosis an exploratory aspira¬ 
tion of the liver may be resorted to without risk if strict 
asepsis be observed. A long needle, not too small in cali¬ 
bre, should be used, and should be deeply inserted in the 
location of the suspected abscess. The aspiration should 
preferably be done under ether. 

Course of Abscess of the Liver.—i. Some abscesses run 
a latent course until rupture occurs. In other cases there 
are found at autopsies old encysted abscesses which gave no 
definite symptoms during the life of the patient. 

2. In some cases the constitutional symptoms are marked, 
but the local symptoms are slight or are altogether absent. 
These cases are often mistaken for typhoid fever, malaria, 
or tuberculosis. 

3. The course may be straightforward, with pronounced 
general and local symptoms. The patient dies from per¬ 
foration or from septicaemia unless the abscess be opened 
and drained. 

4- The abscess may open into the right lung. At the 

37 


578 MANUAL OF THE PRACTICE OF MEDICINE. 

time of rupture there will be raised an expectoration of a 
reddish-brown or brick-dust color, resembling anchovy 
sauce (Osier), in which amoebae coli may be found. 

5. Chronic abscesses may run an insidious course, with 
hectic, loss of flesh and of strength, and slight localized 
pain and tenderness. Amyloid changes in the spleen and 
the kidneys are liable to occur. 

6. In cases of multiple abscesses occurring in the course 
of pyaemia or malignant endocarditis, pain, tenderness, and 
moderate enlargement of the liver may be the only addi¬ 
tional symptoms. 

Diagnosis.—The evident causation of the abscess and the 
character of the pus obtained by aspiration are of prime im¬ 
portance in diagnosis. Abscess of the liver may be con¬ 
founded with the following conditions: 

1. Malarial fever. Here the plasmodium is found in the 
blood, the spleen is enlarged, and the disease yields to qui¬ 
nine. Pain and tenderness over the liver, if present, are but 
slight. 

2. Empyema is to be known by a consideration of its 
cause and by the different appearance of the aspirated pus. 
The heart is displaced, and attendant diseases of the lung 
are evident. It must be remembered that abscess of the 
liver may rupture into the pleural cavity and constitute a 
genuine empyema. 

3. Intermittent hepatic fever with gall-stones. Here the 
clinical picture may closely resemble abscess; but pain is 
more sudden and intense, jaundice is marked, and the fever 
is shorter in duration and is interrupted by periods of apy- 
rexia. Septic symptoms and failure in general nutrition do 
not occur. 

4. Abscess of the abdominal ivall is diagnosed by the incon¬ 
siderable depth of the abscess upon operation. 

5. Snbphrenic abscess is diagnosed by its etiology (rupture 


NEW GROWTHS OF THE LIVER. 


579 


of an ulcer of the stomach or of the duodenum, etc.) and by 
the frequent addition of air or gas to the purulent effusion. 

The prognosis is bad unless the pus be evacuated spon¬ 
taneously or by operation. Multiple small abscesses are 
usually fatal. Single abscesses treated surgically show a 
mortality rate of only 30 per cent. Perforation into the 
lung or into the gastro-intestinal tract is followed by re¬ 
covery in about half the cases. 

The treatment is essentially surgical, consisting in the 
opening and draining of the abscess-cavity. Operative in¬ 
terference is not usually justifiable in cases of multiple 
pyaemic abscesses, and the operation may be postponed if 
perforation into the lung or into the gastro-intestinal tract 
occur, with good drainage, as in these instances spontaneous 
cure may follow. 

TUBERCULAR DISEASE OF THE LIVER. 

1. Miliary tubercles in the liver occur almost constantly 
with miliary tuberculosis, but they give rise to no symptoms. 

2. Large tubercular deposits and cheesy masses may 
occur, usually in connection with tubercular disease of the 
intestines or of the mesenteric glands, but they are chiefly 
of pathological interest. 

3. In the chronic forms of tubercle in the liver there may 
be an increase of connective tissue. This “ tubercular cir¬ 
rhosis,” as it is sometimes called, occurs especially with 
chronic tubercular peritonitis and perihepatitis, and gives 
rise to the symptoms of portal obstruction. 

NEW GROWTHS OF THE LIVER. 

1. Cavernous angioma is not uncommon, but usually is 
of no practical significance. Exceptionally, in children, 
angioma may form a growth of considerable size. 

2. Adenoma may develop; it runs a benign course, 


580 MANUAL OF THE PRACTICE OF MEDICINE . 

although in some instances it seems to merge into car¬ 
cinoma. 

3. Leuksemic deposits will be considered in the descrip¬ 
tion of Leukaemia. 

4. Sarcoma may occur. This affection is usually second¬ 
ary, the skin, the eye, and the bones being the favorite 
seats of the primary growth. Melanotic sarcoma is not 
infrequent. Sarcoma usually develops in small nodules 
generally distributed throughout the liver, and the clinical 
course is that of cancer. 

5. Cancer of the liver may be primary or secondary. The 
primary form, which is exceedingly rare, arises from the 
epithelium of the bile-ducts. It is three times as common 
in women as in men, and it is usually associated with biliary 
calculi. Secondary cancer in the liver may follow—(1) any 
cancer in the distribution of the portal vein, especially in 
the rectum and the stomach; (2) direct extension from 
cancer of the pylorus, colon, pancreas, or omentum; (3) 
more rarely secondary involvement of the liver complicates 
cancer in other organs at a distance. 

Cancer of the liver is more frequent in women than in 
men, and is more common in advanced life. 

Pathology. —There may be one large growth surrounded 
by smaller deposits, or small nodules may be more gener¬ 
ally distributed throughout the liver. These nodules may 
be sharply defined or may fade imperceptibly into the sur¬ 
rounding liver-tissue. Growths near the surface may be 
flush with it or may project as round or flattened nodules, at 
times presenting a central crater-like depression, the so- 
called “ umbilicated appearance.” Hemorrhages may occur 
into the nodules, and there is a tendency to fatty degenera¬ 
tion of the cancer-cells. There is an infiltrating form in 
which small cancer-masses, varying in size from 3 to 10 
millimeters in diameter, are scattered throughout the liver, 


ne w growths of the liver. 


581 

surrounded by fibrous tissue. The appearance of such a 
liver closely resembles that of cirrhosis. Symptoms of 
portal obstruction may or may not be present, according to 
whether or not the growths happen to press on the portal 
vein. Large or multiple growths may thus exist without 
the slightest symptom of portal pressure. In a little less 
than half the cases there is associated a catarrhal inflamma¬ 
tion of the bile-ducts, with jaundice. 

Symptoms. In cases in which the secondary growths are 
small neither mechanical nor functional symptoms are pre¬ 
sented, and the disease runs a latent course. This clinical 
form occurs especially in cases in which the symptoms of 
the primary growth are marked. Should the disease run a 
more classical course, the symptoms of the cancer in the 
liver are pieceded usually by those of the primary growth. 
When secondary deposits occur in the liver, the primary 
cancel, especially if it be in the intestines or in the rectum, 
is apt to cease developing and may be overlooked. Many 
so-called “primary” cancers of the liver are found to be 
secondary to a small quiescent cancerous nodule in the 
rectum. 

The symptoms of cancer of the liver may be classified as 
follows : 

1. There are present the symptoms of a functional disturb¬ 
ance of the liver. 

2. Symptoms of the cancer itself are local and general. 

Local symptoms consist of pain and tenderness. The pain 

is usually steady and severe, with paroxysms running 
through the liver to the back, and at times to the right 
shoulder. Tenderness is usually marked. 

The general symptoms are those of cancerous cachexia. 
The temperature shows a slight elevation in some cases to 
ioo° or 102 0 F., and may be intermittent with rigors. 
There is usually some oedema of the feet, the face is of a 


582 MANUAL OF THE PRACTICE OF MEDICINE. 

waxy pallor, and loss of flesh and of strength becomes 
progressive. Should the local symptoms be slight, the 
general cachexia may be mistaken for that of anaemia or 
of nephritis. There is usually gastric disturbance, with loss 
of appetite, nausea, and vomiting. The cachectic condition 
rapidly becomes marked, as the patient has usually suffered 
for some time from the primary growth, and in some cases 
the cachexia may even precede the enlargement of the liver. 

3. Symptoms of portal obstruction may or may not be 
present, as previously explained. Ascites is uncommon, 
but it may result either from portal obstruction or from can¬ 
cerous disease of the peritoneum. An enlargement of the 
spleen occurs in about half the cases. 

4. Jaundice is present in less than half the cases. The 
symptom is rarely severe, except in occasional acute attacks. 
The beeswax appearance of the skin may resemble jaundice, 
but the conjunctivae and the urine are not discolored. 

Physical Examination.—The liver is regularly enlarged, 
especially in cases of multiple growths, and in extreme cases 
may extend from the third rib to the iliac spines. Usually, 
however, the enlargement does not extend below the umbil¬ 
icus. The margin of the liver is irregular and nodular, and 
the contour of the lower border can usually be distinctly 
appreciated by palpation. The nodular edge moves during 
inspiration and is continuous with the liver-dulness, thus 
distinguishing it from the tumor-like feeling of a rolled-up 
omentum or from growths or cysts of the pancreas. 
Growths of the pancreas may, however, become adherent to 
the liver, so that a positive diagnosis cannot be made in 
every case. The nodules upon the surface of the liver may 
often be felt through the abdominal wall, and in clear-cut 
cases the central depression may be appreciated. The infil¬ 
trating form—“ cancer with cirrhosis ” (Osier)—may lead to 
much enlargement of the liver, and the outlines may be 


HYDATID OF THE LIVER. 


5S3 


Symmetrical. Tenderness is rarely absent, and is of much 
diagnostic value. The spleen is enlarged in half the cases, 
and there may be the physical signs of a slight amount of 
ascites. Important aid in diagnosis is afforded by the detec¬ 
tion of the primary growth. Primary cancers of the stomach 
or the oesophagus usually make themselves evident, but 
primary growths in the rectum and in the intestines may 
easily be overlooked. A rectal examination should be made 
in every case of an enlarged and tender liver in which the 
diagnosis is obscure. 

The duration of cancer of the liver is rarely over one 
year; it may even be shorter than this, as the liver may be 
involved late in the course of primary visceral cancer else¬ 
where. As a practical rule, cancer may be excluded if a 
patient with an enlarged liver be in fair condition at the end 
of a year. 

The prognosis is invariably fatal. 

Treatment is symptomatic. Opium may be given freely 
to relieve the pain. 

HYDATID OP THE LIVER. 

Etiology and Synonym.—The echinococcus is the larval 
stage of the tapeworm, taenia echinococcus, found in the 
intestine of the dog and the wolf. The adult worm, which 
is 4 or 5 millimeters in length, consists of a head with 
four suckers, a double row of hooklets, and four links; 
the last link, being alone mature and containing the eggs, 
is thrown off in the dejecta, and contaminates the food or 
the drink taken by man. The disease is very common in 
Iceland, where dogs are allowed great household privileges, 
one-seventh of all deaths in that country being due to 
hydatid disease. In Australia and in Europe the disease is 
not uncommon, but it is exceedingly rare in America. 
Synonym: Echinococcus cyst. 


584 MANUAL OF THE PRACTICE OF MEDICINE. 

Pathology.—Entering the intestine by contaminated water 
or food, the embryo is carried by the portal vein to the liver, 
where it may lodge ; or it may pass through the liver, enter 
the vena cava, and become lodged in more distant parts. 
In the liver it grows to form a cyst which may be unilocular 
or multilocular. The cyst-wall is composed of two distinc¬ 
tive layers—an outer layer, of a fine, structureless, laminated 
membrane peculiar to hydatid cyst, and an internal granu¬ 
lar layer, the “ endocyst.” In time, surrounding the cyst 
there is gradually developed a capsule of connective tissue. 
The cyst is filled with a clear, non-albuminous fluid contain¬ 
ing sodium chloride and a trace of sugar; the specific gravity 
of this fluid varies between 1005 and 1015. After the cyst 
has grown for from four to six months and has attained the 
size of a walnut, there develop from the inner granular layer 
little pediculated vesicles, the walls of which are identical 
with those of the primary cyst, and which are known as 
“ brood-capsules.” These brood-capsules contain a number 
of echinococcus heads or “ scolices.” Each scolex, consist¬ 
ing of a head, suckers, and hooklets, may project into the 
cavity of the brood-capsule or may retract or invaginate 
itself so as to form a prominence upon the outer side of the 
capsule. Cysts may form within the parent-cysts (daugh¬ 
ter-cysts), and smaller cysts (granddaughter-cysts) may 
develop within these. Some of the cysts may be sterile, 
containing no scolices. The daughter- and granddaughter- 
cysts may remain connected with the ancestral cyst-wall, 
but in time they tend to free themselves. Free hooklets are 
often found; they are of absolute diagnostic value when de¬ 
tected in the fluid obtained by an exploratory aspiration. 

In the multilocular form of hydatid disease the secondary 
cysts are surrounded with fibrous tissue, so that there is 
formed a large irregular tumor of connective tissue arranged 
in septa, enclosing spaces in which are found the cysts; 


HYDATID OF THE LIVER . 


585 

these spaces may also contain gelatinous material. The cysts 
are usually sterile. The peculiar characteristics of the mul- 
tilocular form are attributed to the growth of the brood-cap¬ 
sules outward (exogenous cysts) into the tissues of the liver. 

The growth of hydatid cysts is exceedingly slow, ex¬ 
tending over many years. In some cases spontaneous cure 
occurs—a connective tissue capsule is formed, the cyst-wall 
becomes calcified, and the contents become putty-like and 
may contain free hooklets. In other cases rupture may 
occur in any direction. In a few cases the cyst suppurates 
and assumes the character of an abscess of the liver. 

Symptoms.—In the majority of cases the symptoms are 
purely mechanical, due to the enormous enlargement of the 
liver, and consist of a sense of weight and dragging and of 
dyspnoea. There may be pressure on the portal vein, with 
symptoms of its obstruction—enlargement of the spleen, 
gastro-intestinal disturbances, and ascites. Pressure on the 
bile-ducts causes obstructive jaundice. Pressure on the 
vena cava may result in oedema of the legs. Suppuration 
of the cysts is attended by the symptoms of pyaemia and 
of abscess of the liver. In the multilocular variety portal 
obstruction and jaundice are not uncommonly observed. 
Rupture into the pericardium, the pleura, the peritoneum, 
the gall-bladder, or the vena cava is usually attended by a 
fatal result. Rupture into the lung may allow of partial 
drainage of the cyst, or may be complicated by pneumonia, 
abscess, or gangrene of the lung. Recovery may also fol¬ 
low rupture into the alimentary tract or through the abdom¬ 
inal wall. 

Physical Examination.—There is usually considerable 
bulging in the epigastrium or in the hypochondrium. The 
liver is much increased in size, so that it may extend from 
the second rib to the pelvis. The enlargement, however, is 
not uniform, so that the outline of the liver is exceedingly 


586 MANUAL OF THE PRACTICE OF MEDICINE. 

irregular. Deep-seated cysts give rise to an elastic feeling 
on palpation; superficial cysts give rise to fluctuation. 
Usually the surface of the tumor is smooth and free 
from all irregularities. An “ hydatid fremitus, resembling 
the quivering of jelly, may be detected. According to 
Murchison, this fremitus is not due to the striking of a 
daughter-cyst against the parent-wall, as it may be detected 
in barren hydatids, but may be elicited over any large cyst 
with thin, tense walls and fluid contents; however, as the 
only cysts occurring in the liver with these characteristics 
are hydatids, the fremitus is of much diagnostic value. Un¬ 
fortunately, the sign is not always present. Exploratory aspi¬ 
ration renders the diagnosis positive from the character of 
the watery contents, by the presence of free hooklets, and 
by the occasional presence of small rolled-up bits of the 
outer laminated membrane. 

The prognosis is rendered grave by the possible compli¬ 
cations that may ensue. 

Treatment is entirely surgical. The older methods of 
treatment by aspiration and the injection of iodine have 
been abandoned altogether. 

FATTY LIVER. 

Two varieties of fatty liver are recognized—fatty infiltra¬ 
tion, in which the fat is derived from some constituent of 
the food, and fatty degeneration, in which the fat is due to 
changes occurring within the liver-cell. The latter form 
occurs with phosphorus-poisoning, yellow fever, and acute 
yellow atrophy of the liver. 

Etiology.—Fatty liver may be physiological after a 
hearty meal and during lactation. The disease occurs with 
habitual over-eating, especially of fatty and starchy food, 
with intemperance (frequently associated with cirrhotic 
changes), and with indolent and sedentary habits, especially 


FATTY LIVER. 587 

in those who over-eat. It is common with cachectic con¬ 
ditions and wasting diseases in which the oxidation-pro¬ 
cesses are defective. Thus it frequently occurs with phthi¬ 
sis and with profound anaemias, and less commonly with 
rickets. The disease occurs at all ages, and is more 
common in females than in males. 

Pathology.—The liver is enlarged to such an extent that 
its lower border usually reaches the umbilicus; it may even 
be larger than this. The margins are rounded, and the organ 
shows a greasy appearance. The specific gravity of the 
liver may be so low that the organ will float in water. Cut 
sections are anaemic and of a yellowish color, and the knife 
is smeared with fat \ the stroma is normal. The lesion may 
be complicated by catarrhal inflammation of the bile-ducts. 

Symptoms.—The disease may run a course without 
symptoms, or there may be disturbances in the functional 
activity of the liver, with a sense of weight and fulness in 
the hypochondrium. In some cases there is pain when the 
patient lies upon the left side, from the mechanical stretch¬ 
ing of the peritoneal ligaments. Portal obstruction, marked 
jaundice, and pain and tenderness are absent in this disease. 
In exceptional cases, however, fatty liver does not run the 
benign course usually ascribed to it, but becomes a formid¬ 
able disease. 

1. In some cases the symptoms of functional disturbance 
are marked, symptoms of fatty heart are present, and there 
is a chronic gastritis, possibly with attacks of haematemesis. 
The patient becomes emaciated and dies exhausted. These 
cases somewhat resemble cancer of the liver, but are unac¬ 
companied by pain. 

2. Other patients at some time develop acute gastritis of 
a severe type, with cerebral symptoms, weak heart, and 
possibly haematemesis. These attacks of gastritis are fre¬ 
quently fatal. 


588 manual of the practice of medicine. 

3. Symptoms of a malignant jaundice may develop, al¬ 
though the autopsy fails to reveal obstruction of the bile- 
ducts. These attacks of jaundice resemble those occurring 
in the latter stages of biliary cirrhosis, and are usually fatal. 

Physical Examination.—The liver is symmetrically en¬ 
larged, but it rarely reaches below the umbilicus, as does 
the waxy liver. The organ is soft and smooth on palpation, 
and the lower edge is distinctly rounded. There is neither 
ascites nor enlarged spleen. Examination is frequently 
unsatisfactory because of the obesity of the patient. 

The prognosis is bad for recovery, but the patient may 
live for years. The fatty liver of wasting diseases may 
hasten the fatal issue by interfering with the patient’s nutri¬ 
tion. The occurrence of fatal gastritis or jaundice must 
always be considered in giving a prognosis. 

The treatment is that of the original cause. Exercise is 
to be regulated and enforced in those indolently inclined; 
the use of fat, sugar, and starch should be restricted, and a 
diet of lean meat, green vegetables, and milk is to be recom¬ 
mended. Indulgence in alcoholic or malt liquors is to be 
prohibited. The medicinal treatment is that of functional 
disturbance of the liver. In phthisical patients the condition 
of the liver should not be treated, but superalimentation, 
especially by means of fat, cream, and cod-liver oil, should 
be continued notwithstanding the effect of such a diet upon 
the fatty infiltration of the liver. 

AMYLOID LIVER. 

Etiology and Synonyms.—This condition arises from 
long-continued suppuration, especially of the lungs or the 
bones. It occurs with constitutional syphilis, it may follow 
rickets or prolonged convalescence from infectious fevers, 
and it may complicate cancerous cachexia. Synonyms: 
Waxy liver; Lardaceous liver. 


JAUNDICE. 


589 

Pathology.—The liver is symmetrically enlarged, the 
lower border being frequently found below the navel. The 
organ is firm and hard; its lower edge is sharp. The 
cut section is anaemic, and in places shows a translucent 
appearance resembling raw bacon. The amyloid areas are 
stained mahogany-brown by dilute watery solutions of 
iodine. The amyloid change begins first in the small blood¬ 
vessels and extends to the connective-tissue stroma. The 
liver-cells do not become waxy, but they may be atrophied 
by pressure or may undergo fatty degeneration. Similar 
waxy changes are found in other viscera, especially in the 
spleen and the kidney. 

Symptoms.—There are no characteristic symptoms. 
Jaundice does not occur. There is no portal obstruction, 
unless the portal vein be compressed by an enlarged waxy 
gland in the hilum of the liver. 

Physical examination reveals a symmetrical painless 
enlargement of the liver. As the patient is usually emaci¬ 
ated, the detection of the enlargement is never difficult, and 
the sharp lower edge may be appreciated distinctly. The 
spleen is enlarged, and the waxy condition of the kidney 
is made evident by the passage of an increased amount of 
urine containing albumin, and generally by oedema of the 
lower extremities. 

Prognosis and treatment are those of the causative 
disease. 


JAUNDICE (ICTERUS). 

Etiology.—Two varieties of jaundice are described. The 
first, the obstructive or hepatogenous jaundice, is due to 
obstruction of the bile-ducts and results from the absorption 
of the bile-pigments. The second or hcematogenous variety 
includes those cases of jaundice in which no obstruction 
exists. The causes of jaundice are thus classified: 


590 MANUAL OF THE PRACTICE OF MEDICINE. 

1. Obstructive or Hepatogenous Jaundice. — (a) Foreign 
bodies within the duct—gall-stones, inspissated bile, para¬ 
sites, and bodies entering from the duodenum. 

(, b ) Catarrhal inflammation of the bile-passages or of the 
duodenum. 

(r) Stricture or obliteration of the common duct, congenital 
and cicatricial. 

(d) Pressure on the duct from without —(i) from enlarged 
glands in the hilum of the liver ; (2) from neighboring tumor, 
as of the liver, stomach, or pancreas; (3) from large abdom¬ 
inal tumors, as aneurysm of the abdominal aorta, fecal 
impaction, ovarian tumor, and pregnancy; (4) from con¬ 
tracting peritoneal bands and thickening ; (5) from lowering 
of the blood-pressure in the liver so that it is less than the 
pressure of the bile within the smaller ducts, as in mental 
shocks and cerebral concussion. 

2. Non-obstructive or Hcematogenous Jaundice. —The fol¬ 
lowing classification is given by Osier: 

(a) From widespread necrosis of liver-cells, interfering 
with their bile-forming function, as in acute yellow atrophy 
and in certain cases of hypertrophic cirrhosis. 

(b) The toxic form. The poisons of yellow fever, Weil’s 
disease, malaria, typhoid fever, epidemic jaundice, pyaemia, 
snake-bites, chloroform, ether, phosphorus, and mercury 
cause such an increased destruction of the blood-cells 
(haemolysis) that more blood-pigment is set free than can 
be eliminated, and is retained in the tissues. 

Symptoms.—1. Of Hepatogenous Jaundice. —The jaun¬ 
dice first appears in the conjunctivae and the urine, and then 
appears in the skin and the mucous membranes. The color 
of the skin varies from a canary-yellow to an orange-green or 
even to a greenish-black. The constant tinting of the con¬ 
junctivae and the presence of bile-pigment in the urine dis¬ 
tinguish jaundice from all other pigmentations or stainings 


JAUNDICE. 


591 


of the skin. The urine, which is deeply bile-stained and is 
often of a brownish color resembling porter, foams readily, 
and the froth is yellow; it stains linen and reacts to Gmelin’s 
test. The abundant yellow foam distinguishes the urine of 
jaundice from urine discolored by the internal use of rhu¬ 
barb or of santonin. Hyaline tube-casts are not uncommon, 
and in severe or protracted cases there may be a moderate 
amount of albumin in the urine. The perspiration is bile- 
stained and will stain linen, but the saliva, the tears, and the 
milk are not discolored. Pruritus of the skin is severe and 
distressing, especially in protracted cases. Digestive dis¬ 
turbances arise from the fact that no bile passes into the 
intestine. The assimilation of fats is interfered with, so that 
the patient loses flesh and becomes anaemic. There is a 
bitter taste in the mouth; the tongue is heavily furred. 
Abdominal flatulence develops. The bowels are usually 
constipated, although diarrhoea may occur if fermentative 
changes take place within the intestine. The stools are 
clay-colored, pasty, or putty-like, and are usually offensive. 
The heart-action is slower and more forcible than normal, 
in severe cases falling to 40, or even to 20, in the minute. 
The slowness of the pulse is best observed when the patient 
is resting, as the heart-action may become rapid and feeble 
upon exertion. There is no fever with simple jaundice ; on 
the contrary, the temperature is more apt to be subnormal 
—96° or 97 0 F. In severe or protracted cases there is 
developed a tendency toward hemorrhage. Purpuric spots 
and ecchymoses appear beneath the skin and the mucous 
membranes, and hemorrhages from free mucous mem¬ 
branes may occur, especially from the nose, the stomach, 
and the intestines. The hemorrhagic tendency may be so 
extreme as to preclude surgical treatment, as in operations 
the bleeding from the incision may become uncontrollable. 

Cerebral symptoms are almost constant. In mild cases 


592 MANUAL OF THE PRACTICE OF MEDICINE. 

there are persistent headache, irritability of temper, and 
utter inability to concentrate the mind. Severe cerebral 
symptoms resemble those occurring with uraemia, and com¬ 
prise delirium, convulsions, stupor, and coma; or the patient 
may pass into the typhoid condition with hemorrhages. 
The temperature in these severe cases may be as low as 
87° F., but a high ante-mortem rise to 106° or 108° F. is 
commonly observed. To these severe cases with cerebral 
symptoms the names “ pernicious jaundice,” “ cholaemia,” 
“ acholia,” and “ cholesteraemia ” have been given. The 
best explanation of these cases is given by Frerichs, who 
ascribes the toxaemia to the pernicious influence of unknown 
substances which, under normal conditions, should be 
elaborated by the liver into bile. 

2. Of Hematogenous Jaundice .—The symptoms are often 
obscured by those of the primary disease. As a rule, 
the tint of the skin is lemon-colored. The urinary pig¬ 
ments are usually increased, but, as a rule, bile-pigment 
is not found in the urine. As bile enters the intestine, the 
stools do not become clay-colored. The pulse is not gen¬ 
erally lowered in frequency, but in the toxic form severe 
cerebral symptoms are apt to develop. 

The treatment of jaundice as a symptom will be given 
under the heading of Catarrhal Jaundice. 

Acute Febrile Jaundice. 

(See Weil's Disease.) 

Catarrhal Jaundice. 

Etiology and Synonym.—This most common disorder 
is due to the closure of the terminal end of the common bile- 
duct by swelling or by a plug of mucus during the course of 
an acute gastro-duodenitis. The inflammation in some cases 
extends upward along the common bile-duct. The gastro- 


JAUNDICE . 


593 


duodenitis is usually due to some dietetic error. It may 
occur at any age, but it is especially frequent in young 
people. The occurrence of the duodenal catarrh is favored 
by portal obstruction and by chronic heart disease. Such is 
the low tension of the bile within the duct that a very mod¬ 
erate amount of swelling or occlusion prevents the bile from 
entering the intestine and results in obstructive jaundice. 
Synonym: Gastro-duodenitis. 

The symptoms are those of gastritis and of jaundice. 
The gastric symptoms are the first to appear, and begin 
insidiously with malaise, loss of appetite, nausea, and vomit¬ 
ing. The bowels are usually constipated. There may be 
epigastric pain and tenderness. Mild cases are unaccom¬ 
panied by fever, but in the more severe forms there may be 
a temperature of from ioo° to 102° F. After the gastric 
symptoms have lasted for a few days jaundice appears, but 
the deeper greenish-yellow tints are not seen. The regular 
symptoms of jaundice are present, as described in the pre¬ 
ceding article. After about a week the patient begins to 
improve and the gastric symptoms become less marked. 
The jaundice is slower in disappearing, so that the whole 
duration of the disease is usually from four to eight weeks. 
There are mild cases in which jaundice may be the first, 
and even the only, symptom, and the jaundice may termi¬ 
nate within two weeks. 

The diagnosis is usually made with ease. Doubt should 
be attached, however, to those cases in which the jaundice 
persists for over three months. 

The prognosis is good. In exceptional cases gastro- 
duodenitis with jaundice may occur in a patient who has a 
fatty or cirrhotic liver, and may terminate fatally. 

Treatment. —No very active treatment is indicated in the 
mild cases. The patient is better for keeping about, in spite 
of his prominent color. The treatment is in the main that 
38 


594 MANUAL OF THE PRACTICE OF MEDICINE. 

of an acute gastric catarrh. Cholagogues are of great 
service, provided that by their administration the gastritis 
is not aggravated. Of the cholagogues, the best is sodium 
phosphate in 3j doses before meals. Benzoic acid, sodium 
benzoate, sodium salicylate, small doses of rhubarb, and an 
occasional mercurial purge are also recommended. Sodium 
bicarbonate may be given in 3j doses, in Vichy water, 
between meals; or any of the simple alkaline mineral waters 
may be given, of which Vichy is perhaps the best. Rectal 
injections of cold water certainly do good in diminishing 
the jaundice. From I to 2 quarts of water should be slowly 
injected into the rectum once a day, and retained as long as 
possible. At first the temperature of the water should be 
6o° F., but in later injections the temperature of the water 
may be reduced gradually, so that finally ice-water may be 
used. Pruritus is to be treated by bathing the itching parts 
with a solution of carbolic acid (i : 200) or one of bichloride 
of mercury (gr. j : sj); or a saturated solution of sodium 
bicarbonate may be used. In some cases a calomel oint¬ 
ment affords relief. In severe cases internal remedies may 
be necessary, as phenacetine or sodium bromide. 

CHOLELITHIASIS. 

Etiology and Synonyms. —Gall-stones occur more fre¬ 
quently in women (75 per cent, of cases) than in men, and 
especially in women between thirty and sixty years of age. 
Tight lacing, over-eating, especially of saccharine and 
starchy food, and sedentary modes of life seem to act as 
important factors in their causation. The patients are 
usually stout, and the combination of fatty liver with biliary 
calculi is exceedingly common. Of women with gall-stones, 
90 per cent, have borne children. Synonyms : Gall-stones ; 
Biliary calculi. 

Pathology. —Biliary calculi are in almost all instances 


CHOLELITHIASIS. 


595 


formed within the gall-bladder, but in rare cases they may 
arise in the small ducts within the liver. Stones found in 
the larger ducts do not originate there, but become impacted 
on their way to the intestine along the duct. Two varieties 
of biliary calculi are found, one consisting of inspissated 
bile, and the second comprising calculi proper. 

1. Inspissated bile occurs as a brown or greenish-black 
semi-solid mass composed of the solid constituents of bile 
with the admixture of mucus. The same symptoms may 
arise from inspissated bile as from the regular calculi. 

2. The regular biliary calculi are not always composed 
of the same ingredients. 

(a) Some are composed of cholesterin, alone or with bile- 
pigment. 

(b) Some are composed of cholesterin, bile-pigment, and 
the salts of lime and magnesium. These two are the 
ordinary varieties. The calculi are soft, light and can be 
cut easily with a knife. 

(<t) Rarely the calculus consists of bile-pigment alone or 
of calcium carbonate alone. These latter varieties form 
small hard gravel, the so-called “gall-sand.” There is 
usually a central nucleus, which may consist of mucus or 
of bile-pigment. 

The number of calculi that may be found in the gall¬ 
bladder varies up to several thousand. The calculi vary 
in size from a grain of sand to that of a lemon; the greater 
their number the smaller they are. The color varies from 
white to a waxy lemon or a greenish-yellow, according to 
the amount of pigment they contain. More rarely they are 
bronze-green or even black. The purer cholesterin-calculi 
are nearly white, are of a crystallized structure, and readily 
cut like wax. The calculi are round, irregular, or oblong, or 
they may be polyhedral and faceted by mutual pressure and 
friction. 


596 MANUAL OF THE PRACTICE OF MEDICINE. 

The exact reason for the formation of biliary calculi is un¬ 
known. It is a fact that cholesterin is precipitated if the bile 
becomes acid, but whether this precipitation actually occurs 
within the body is unknown. It is supposed that cholesterin 
is also precipitated whenever there exist defects in the sodium 
salts. It is known that the formation of calculi is favored 
by any cause retarding the flow of bile and by all unhealthy 
conditions of the bile-passages. 

Symptoms.—Gall-stones give rise to symptoms in three 
different ways: 

1. By their passage through the ducts; 2. By their impac¬ 
tion in the ducts; 3. By their retention within the gall¬ 
bladder. 

1. Passage through the Ducts .—Small stones may pass 
from the gall-bladder through the cystic and common ducts 
without symptoms, or there may result slight jaundice and 
discomfort in the region of the liver. Larger calculi en¬ 
gaging in the ducts give rise to the symptoms of biliary or 
hepatic colic—pain, vomiting, fever, jaundice, and slight 
enlargement of the liver. The attack is sudden, usually 
occurring several hours after a heavy meal or after muscular 
exertion. The pain starts from the epigastrium and radiates 
through to the back and upward, so that it may be felt in 
the right shoulder. Radiation of the pain downward is ex¬ 
ceedingly rare—a point of differential diagnosis from renal 
colic. There are two elements to the pain—a steady grind¬ 
ing ache, with sharp cutting or stabbing paroxysms of un¬ 
bearable intensity. During the paroxysms of pain the face 
is pale, the body is bathed in perspiration, and attacks 
of syncope and convulsions are not infrequent. Fatal 
syncope or collapse has occasionally been observed. At 
the onset the pain may be relieved by pressure, but later 
tenderness develops, especially over the gall-bladder. Nau¬ 
sea and vomiting almost regularly occur during the attack. 


CHOLELITHIASIS. 


597 


The vomited matters contain no bile if the common duct be 
obstructed, but in the vomita biliary calculi may be found. 
Chills are common at the onset of the attack, and recur at 
intervals which, in protracted cases, may be of such regu¬ 
larity as to resemble malarial fever. The temperature is 
temporarily raised during the attack to 102° or 104° F., but 
if the attack be slight and of short duration there may be no 
fever. In protracted cases, especially if there be a compli¬ 
cating inflammation of the biliary passages, there may be 
an intermittent or remittent fever resembling that of malaria 
and accompanied by repeated rigors. This “ intermittent 
hepatic fever ” also occurs with impaction of the stone with¬ 
in the common bile-duct. 

The pulse during an attack of biliary colic is often slow, but 
it may be rapid, feeble, or irregular. In from twelve to 
twenty-four hours jaundice appears, with the regular symp¬ 
toms of the obstructive variety, but it usually disappears in 
about a week after the close of the attack. Persistence of 
the jaundice after this time suggests catarrhal inflammation 
of the bile-ducts (catarrhal cholangitis) or impaction of the 
calculus within the duct. Jaundice is not, however, con¬ 
stant, as it does not appear in case of a very small calculus 
within the common bile-duct, not entirely occluding it, or in 
the case of a calculus passing the cystic duct. Toward the 
close of the attack the liver is moderately enlarged and 
tender, and the gall-bladder may be felt to be distended. 

The attack terminates suddenly with the dropping of the 
calculus into the duodenum, and the sharp pain ceases at 
once, leaving a dull ache which may persist for several 
days. Sudden cessation of pain is also observed in cases 
in which a calculus engages in the cystic duct and then 
drops back again into the gall-bladder. 

The duration of an attack of biliary colic varies from 
several hours to days. Protracted cases are usually due to 


59 8 MANUAL OF THE PRACTICE OF MEDICINE. 

the merging together of a series of attacks. Recurrences 
are common, because the biliary calculi usually occur in the 
gall-bladder in great numbers. 

The diagnosis of cholelithiasis is rendered positive by 
finding the calculi in the stools or in the vomited matters. 
The stools should be tied up in a gauze bag, which is to be 
attached to a water-faucet so that the feculent matter may be 
washed through the meshes of the gauze, leaving the cal¬ 
culi in the bag. A faceted appearance of a calculus implies 
that it is one of many. 

The prognosis for the attack itself is good, although fatal 
syncope, collapse, and rupture of the duct have occurred. 
Cerebral hemorrhage has repeatedly been observed during 
an attack. 

2. Impaction in the Ducts .—The symptoms of impaction 
follow those cases of biliary colic in which the pain gradu¬ 
ally ceases, leaving a considerable dull aching feeling ; they 
differ according to whether the cystic or the common bile- 
duct be the seat of the impaction. 

(a) Impaction in the Cystic Duct.— There is usually no 
jaundice, but the effects of the impaction fall upon the gall¬ 
bladder, which may undergo the following changes: 

(0 The gall-bladder becomes distended with thin, color¬ 
less, mucoid contents—the so-called “ dropsy of the gall¬ 
bladder," or “ hydrops vesicae felleae.” A large globular 
tumor is thus formed, projecting from the under surface of 
the liver to the right of the median line. The distended 
gall-bladder may reach such dimensions as to extend to the 
navel or even to the level of the anterior spines. In some 
cases the gall-bladder becomes distended without projecting 
beyond the lower border of the liver. 

(2) Acute phlegmonous cholecystitis may occur, with 
perforation and fatal peritonitis, but the condition is one of 
great rarity. 


CHOLELITHIASIS. 


599 


( 3 ) Suppurative cholecystitis, or empyema of the gall¬ 
bladder, is of not infrequent occurrence. The bladder is 
distended by pus and is the source of pain and tenderness. 
Septic symptoms are those of a localized abscess. Perfora¬ 
tion may occur into the peritoneum, into hollow viscera, or 
through the abdominal wall, forming biliary fistulae; or 
there may be formed an acute circumscribed peritoneal 
abscess. Calcification of the gall-bladder or lime-incrusta¬ 
tions of the mucosa may follow the drainage of the em¬ 
pyema. 

(4) Atrophy of the gall-bladder may result in its trans¬ 
formation into a little ball of connective tissue. 

(< b ) Impaction within the common bile-duct causes persistent 
obstructive jaundice. The secondary results of such an 
impaction fall upon the bile-passages and the liver. The 
gall-bladder is seldom involved. 

(1) Inflammation of the Biliary Passages. —There may be 
a catarrhal cholangitis. The biliary ducts are dilated and 
filled with a colorless mucoid fluid. The symptoms are 
those of jaundice with “ intermittent hepatic fever.” Chills 
occur, with elevations in temperature to 103° or 104° F., 
the fall of the fever being accompanied by sweating. These 
ague-like paroxysms may occur with such periodicity as to 
be mistaken for malaria, and they may occur at intervals for 
months or even for years. With each paroxysm the jaun¬ 
dice deepens, and pain over the liver and gastric disturb¬ 
ances are observed. In the intervals between the paroxysms 
the patient is deeply jaundiced, but the temperature is nor¬ 
mal and there is rarely any depreciation in the general 
health. The exact cause for this hepatic fever is not 
known. 

(2) Suppurative cholangitis is attended by suppuration 
extending along the biliary passages and frequently involv¬ 
ing the gall-bladder. Suppuration may extend to the liver 


600 MANUAL OF THE PRACTICE OF MEDICINE. 


surrounding the ducts, so that the organ is penetrated by 
long - , branching; abscess-cavities. The liver becomes en- 
larged and tender, symptoms of septicaemia or of pyaemia 
develop, and the disease runs a short and fatal course. 

The effect on the liver of such an impaction in the common 
duct is to cause its enlargement. The liver is rendered 
firmer by deposits of connective tissue along the course of 
the biliary ducts, and the lesions, of biliary cirrhosis may 
thus ultimately develop. 

When a calculus becomes impacted in either the cystic 
or the hepatic duct, it may there remain indefinitely, or it 
may progress along the duct by starts, so that finally the 
passage to the duodenum is accomplished. This favorable 
outcome of the impaction is more common if several calculi 
are wedged together, so that at any time the wedge may be 
broken up and the individual calculi be passed without 
difficulty. 

Perforation of the duct is of common occurrence, and 
biliary fistulae thus formed may open through the abdominal 
wall, into the abdominal cavity, into the duodenum or the 
colon, more rarely into the gall-bladder, the substance of 
the liver, the lungs, the stomach, the small intestine, or the 
pelvis of the kidney. The calculi may be discharged 
through the fistulous opening, frequently in great num¬ 
bers, and spontaneous cure may result. Obstruction to the 
bowels may result from the perforation of large solitary 
gall-stones into the duodenum. In other cases perforation 
of the duct leads to the formation of a circumscribed peri¬ 
toneal abscess. 

In some instances a calculus may pass into the common 
duct and remain there without actually obstructing the duct. 
A slow increase in the size of the calculus is compensated 
by a gradual dilatation of the duct. 

3. Retention of calculi within the gall-bladder is of such 


CH0LELITH1A SIS. 


601 


common occurrence as to be found in 25 per cent, of all 
autopsies made on women over sixty years of age. In many 
cases this condition gives absolutely no symptoms, but post¬ 
mortem examination may show the gall-bladder nearly 
empty of bile and contracted upon the calculi, with oblitera¬ 
tion of the cystic duct by a calculus. In the majority of cases, 
however, calculi from time to time enter the cystic duct and 
pass to the duodenum or drop back into the gall-bladder. 
In either case symptoms of biliary colic are observed, but 
in the latter instance jaundice does not occur and the pain 
may be of short duration. Calculi remaining in the gall¬ 
bladder may excite a catarrhal or suppurative inflammation 
of its wall. Catarrhal cholecystitis is attended by a globu¬ 
lar enlargement of the gall-bladder, with pain and tender¬ 
ness. The symptoms of empyema of the gall-bladder have 
already been described. 

Treatment of Cholelithiasis.— 1. During the attack of 
biliary colic the indications are to relieve pain and spasm. 
A hot bath is of comfort, and until the bath can be pre¬ 
pared hot applications over the liver are of service. Hypo¬ 
dermic injections of morphine (gr. £) with atropine (gr. ^) 
are to be given, and in severe cases whiffs of chloroform 
may be necessary until the patient is under the effect of the 
opiate. It should be remembered that the pain may cease 
suddenly, and, tolerance for the morphine being thus les¬ 
sened, toxic effects may result if too large doses have been 
given. Copious draughts of hot water containing sodium 
bicarbonate (3j : Oj) exert a sedative effect, provided that 
vomiting is not induced. 

2. If the ducts be occluded, various methods have been 
recommended to dissolve the calculus or to dislodge it 
mechanically. Olive oil in large doses has been recom¬ 
mended, but it is useless, the alleged calculi passed after its 
administration having been proved to be lumps of fatty 



602 manual of the practice of medicine. 


concretions. Durande’s formula, consisting of 3 parts of 
ether and 2 parts of turpentine, may be given in from 15- to 
20-drop doses three times a day. It is much used by 
European physicians, but is of doubtful utility. Chloroform 
internally and salicylate of soda have been recommended, 
but no drug thus far has proved to be of any value in dis¬ 
solving the stone. 

If the impaction be accompanied by inflammatory symp¬ 
toms, the stone may be removed surgically, or the duct 
may be exposed and the calculus be broken up without 
incising the wall of the duct. 

3. If empyema of the gall-bladder occur, the condition 
demands surgical treatment. For cases of repeated attacks 
of gall-stone colic, with accumulations of calculi in an 
inflamed gall-bladder, the operation of cholecystotomy, or 
opening the gall-bladder and removing the stones, has been 
remarkably successful. 

Dropsy of the gall-bladder may be treated by repeated 
aspirations. 

To prevent the formation of gall-stones, highly seasoned 
and indigestible food should be avoided, and total absti¬ 
nence from alcohol should be insisted upon. The bowels 
should be kept freely open, and abundant systematic exer¬ 
cise should be enforced. Hot morning draughts of the 
alkaline mineral waters are of service, or sodium phosphate 
in dram doses may be given in a tumblerful of hot water 
before breakfast. 

CANCER OP THE GALL-DUCTS. 

Cancer of the liver starting from the endothelium of the 
biliary passages has already been described. 

The common bile-duct in rare instances is the seat of the 
primary cancer. The symptoms are those of chronic 
obstructive jaundice and of cancerous cachexia. The diag- 


DISEASES OF THE BLOOD-VESSELS OE THE LIVER. 603 

nosis is seldom, if ever, made during life, and no treatment 
is available except that for the relief of pain. 

Cancer of the gall-bladder is also exceedingly rare. The 
tumor reaches considerable size, usually that of a child’s 
head. 

Secondary nodules in the liver occur by direct extension 
or by metastasis through the portal vein. The symptoms 
are those of an enlarged, tender, and painful tumor in the 
location of the gall-bladder, of secondary growths in the 
liver, and of cancerous cachexia. The early symptoms 
resemble those of gall-stones. Treatment is palliative, 
unless an early diagnosis renders it possible to remove the 
gall-bladder by operation. 

DISEASES OP THE BLOOD-VESSELS OF THE 

LIVER. 

Hepatic Artery.—Aneurysm of the hepatic artery has 
been observed in a few cases. There may be pressure on 
the portal vein or on the bile-ducts. 

Hepatic Vein.—Affections of the hepatic vein are almost 
unknown. 

Portal Veins.— 1. Chronic portal obstructio 7 i may arise 
from chronic diseases of the heart and the lungs and from 
tumors of the mediastinum pressing upon the vena cava. 
The portal obstruction thus caused is accompanied by 
oedema of the lower extremities and by congestion of the 
kidney. 

Local causes for portal obstruction are cirrhosis, throm¬ 
bosis, and pressure on the vein by tumors in the liver or in 
its vicinity. The vein may be compressed by proliferative 
peritonitis involving the grastro-hepatic omentum. 

The symptoms and treatment of chronic portal obstruction 
have been described at length in the consideration of Cir¬ 
rhosis of the Liver. 


604 manual of the practice of medicine. 

2. Thrombosis; Adhesive Pylephlebitis. —Primary throm¬ 
bosis of the portal vein may occur as a terminal event in 
dying patients, but it is of no practical importance. Sec¬ 
ondary thrombosis is regularly due to pressure upon the 
portal vein or upon one of its branches. 

Pathology. —The vein is filled with a recent clot; later the 
thrombus becomes paler and harder, and may ultimately be 

converted to connective tissue. 

The symptoms are those of sudden portal obstruction. 
The abdominal veins become distended; the spleen is en¬ 
larged ; vomiting, hsematemesis, diarrhoea, occasionally with 
bloody stools, and rapidly forming ascites comprise the 
prominent symptoms. In no other disease are these symp¬ 
toms of portal obstruction so rapidly developed. 

If the portal vein itself or one of its larger branches be 
occluded, an efficient collateral circulation is impossible. 
Death results in a few days from prostration and heart fail¬ 
ure, which are added to the above-mentioned symptoms. 
If the collateral circulation can be established, a certain 
amount of improvement results, and the patient may live 
for years with indefinite symptoms of moderate portal stasis , 
but death finally results from emaciation, from exhaustion, 
or from hemorrhages. 

The prognosis of thrombosis of the larger branches of the 
portal vein is always bad. If a smaller branch be occluded, 
the prognosis depends upon the establishment and mainten¬ 
ance of satisfactory collateral circulation. 

The treatment is that of portal obstruction by tapping, 
diuretics, and cathartics. 

3. Septic Thrombosis; Suppurative Pylephlebitis. —The 
thrombus is not due to mechanical pressure, but is second¬ 
ary to a septic inflammation of the wall of the vein. Infec¬ 
tion is caused by intestinal ulceration, by abdominal ab¬ 
scesses, or by sharp foreign bodies, as fish-bones, which 


DISEASES OF THE PANCREAS. 605 

penetrate the wall of the intestine and infect a branch of the 
portal vein. In new-born children the condition may arise 
from sepsis entering through the navel and infecting the 
clot in the umbilical vein. 

Pathology .—By the influence of bacteria the clot softens 
and breaks down to form a puriform mass. Septic emboli, 
entering the liver, give rise to multiple abscesses, and even 
to general pyaemia. 

The symptoms are those (1) of portal obstruction, (2) of 
multiple abscesses in the liver, and (3) of pyaemia or septi¬ 
caemia. 

Prognosis .—The disease is invariably fatal, usually within 
two weeks. 

The treatmejit is symptomatic. Operative interference is, 
of course, impossible. 


6. DISEASES OF THE PANCREAS. 

HEMORRHAGE. 

Hemorrhage into the pancreas is of rare occurrence. The 
subjects have usually been males of adult life. Injuries and 
alcoholism seem to bear some causative relation to the dis¬ 
ease, but the precise causation is unknown. 

Pathology.—Hemorrhagic infiltration is found not only 
in the substance of the pancreas, but also in the subperi- 
toneal tissue in its vicinity. 

Symptoms.—There is suddenly developed intense pain, 
referred to the upper part of the abdomen; nausea, vomit¬ 
ing, and abdominal tenderness rapidly follow. The patient 
becomes anxious, restless, and passes into a fatal collapse. 
In the rapidly fatal cases death may result in from half an 
hour to two hours. In less severe cases the symptoms 
merge into those of hemorrhagic pancreatitis. 



606 MANUAL OF THE PR A C TICE OF MEDICINE , 


Prognosis. —Theoretically it is possible for recovery to 
follow small hemorrhages, but practically the disease is 
almost certainly fatal. 

Treatment is directed toward the pain and the collapse. 

ACUTE HEMORRHAGIC PANCREATITIS. 

Etiology. —The subjects of pancreatitis are usually males 
in adult life. The majority of the reported cases have been 
preceded by hemorrhage into the pancreas, by alcoholism, 
by injury to the abdomen, or by repeated attacks of gastro- 
duodenitis, but the precise causation of the disease is 
unknown. 

Pathology. —The pancreas is enlarged and is infiltrated 
with blood. The color of the gland is mottled red and 
yellow and dead white. The latter color is due to areas of 
“ fat-necrosis ” of Balser. 1 The same lesions may also be 
found in the root of the mesentery, in the mesocolon 
and the omentum, and in the retroperitoneal tissues in the 
vicinity of the pancreas. If the patient survive long enough, 
gangrenous pancreatitis may develop. 

The tallow-like appearance of the areas of fat-necrosis is 
due to the crystallization of fat, as the area is found to con¬ 
sist of stearin, alone or combined with lime-salts. The 
crystallization is supposed to be due to contact with the 
pancreatic secretion. In the areas of fat-necrosis various 
bacteria have been found, the most prominent being the 
bacillus coli communis. 

The symptoms begin suddenly with an intensely violent 
pain, usually referred to the upper abdominal region, but 
which may be more general than this. Vomiting is fre¬ 
quent and usually incessant. The vomited matters are 

1 Disseminated areas of fat-necrosis may in rare instances be scattered 
throughout the abdomen, even in cases in which the pancreas is found to be 
normal. 


GANGRENOUS PANCREATITIS. 60? 

bilious and may contain blood. The temperature may be 
normal, subnoi mal, or slightly elevated. The bowels are 
usually constipated. The abdomen becomes tympanitic 
and tender. Collapse-symptoms rapidly supervene, and 
death usually results from the second to the fourth day. 
Should the patient survive, the symptoms of gangrenous 
pancreatitis usually appear. 

The diagnosis from intestinal obstruction and from per¬ 
forative peritonitis cannot be made with any certainty. 

Prognosis. —The disease is almost certainly fatal, although 
one case of recovery has been reported by Osier. 

The treatment is that of the pain and the collapse. 

GANGRENOUS PANCREATITIS. 

According to Fitz, hemorrhagic pancreatitis not ter¬ 
minating fatally or in improvement within a week usu¬ 
ally results in gangrenous pancreatitis. The pancreas is 
converted to a gangrenous mass lying in a meshwork 
infiltrated with green offensive fluid; or the sloughing mass 
may lie in the lesser omental cavity, attached only by a few 
loose threads to its walls, and may be discharged through 
the bowels as a slough. In rare cases spontaneous cure 
has thus resulted. The omental cavity contains an ichorous 
fluid or pus, and general infection of the peritoneum may 
occur. Disseminated areas of fat-necrosis are usually pres¬ 
ent, and there may be suppurative pylephlebitis, pericarditis, 
or pleurisy. 

Symptoms. —The disease begins as a hemorrhagic 
pancreatitis. Symptoms of peritonitis supervene, usually 
localized in the upper portion of the abdomen, correspond¬ 
ing to the omental cavity. Collapse precedes the fatal issue. 

The duration of the disease is from ten to twenty days. 

The prognosis is bad, with the exception of the very rare 
cases in which the slough is passed by the bowel. 


608 MANUAL OF THE PRACTICE OF MEDICINE. 

The treatment is that of a circumscribed peritonitis, and 
is distinctly surgical. 

SUPPURATIVE PANCREATITIS. 

Etiology. —The method of infection is unknown. 

Pathology—The pancreas may be studded with small 
abscesses or may be converted to a cyst filled with pus. A 
diffuse peritonitis may result, or the abscess may luptuie 
into the lesser omental cavity or into the duodenum. Sup¬ 
purative pylephlebitis and abscesses in the liver are not 
infrequent. Areas of fat-necrosis are but rarely observed. 

Symptoms. —Epigastric pain, vomiting, and prostration 
mark the onset of the disease. Septic symptoms develop, 
abdominal distention and tenderness become marked, and 
death results in from two to four weeks. Other cases run 
a more chronic course extending over weeks or months. 
Fever is slight or altogether absent. There is but little 
pain, although tenderness is elicited in the region of the 
pancreas. The patient becomes weak and thin, and dies 
exhausted in from six to twelve months. 

The prognosis is invariably fatal. 

The treatment is surgical. 

CHRONIC PANCREATITIS. 

Etiology.—This condition may be due to congenital 
syphilis, but, with this exception, little is known as to the 
etiology of the disease. 

Pathology.—The pancreas may be enlarged or diminished 
in size. There is a great increase in the interstitial connec¬ 
tive tissue, and the glandular structure may become changed 
or atrophied. 

Symptoms. —There are no characteristic symptoms. 
There are commonly present digestive disturbances resem¬ 
bling those of chronic gastro-enteritis. The stools may be 


PA NCREA TIC C VS IS. 


609 

fatty. Jaundice is present in some cases, and is due to the 
pressure of the enlarged pancreas upon the common duct. 
There may be considerable epigastric pain and tenderness, 
and in some cases a sense of resistance can be appreci¬ 
ated over the pancreas. Emaciation and debility become 
progressive. In some cases glycosuria has been observed, 
and the disease may run the course of a severe diabetes. 
Ascites may develop in advanced cases. 

The disease is chronic, but, from the insidious character 
of the symptoms presented, the precise duration of the 
disease cannot be determined. 

The prognosis is grave, but not hopeless. 

The treatment is to be supporting. The general nutri¬ 
tion of the patient should be improved in every possible 
way, and pancreatin or minced pancreas may be given, as 
indicated in all cases of diminished pancreatic digestion. 

PANCREATIC CYSTS. 

Retention-cysts may arise from the occlusion of Wir- 
sung’s duct by biliary or pancreatic calculi. The latter con¬ 
sist mainly of carbonate of lime. The duct may be obliter¬ 
ated by pressure from without or by cicatricial contraction. 
In rare cases cystomata may occur and may merge into 
malignancy. 

Pathology. —The cysts, which may be single or multiple, 
are filled with an alkaline grayish fluid which emulsifies fats, 
converts starch into glucose, and, more rarely, digests albu¬ 
min. These characteristics, however, are not peculiar to 
pancreatic cysts, and the older the cyst is, the less likely is 
the fluid to present these reactions. Hemorrhages into the 
cyst are common, so that the fluid becomes bloody or of a 
brown or chocolate color. 

The symptoms are chiefly those of an abdominal tumor, 
which is of globular form, resistant and smooth, and in some 


6 10 MANUAL OF THE PRACTICE OF MEDICINE . 

cases fluctuating. "1 he tumor first presents itself in the 
epigastrium or in the left hypochondrium, but may extend 
to fill the entire abdominal cavity. There may be a decep¬ 
tive pulsation which is transmitted from the aorta. Pain 
is inconstant. There may be symptoms of pressure on the 
portal vein and on the bile-ducts, and cases of fatal lupture 
have occurred. 

The growth of the cyst may be apparent in three weeks, 
but usually the course is chronic and extends over months 
and years. A sudden enlargement is suggestive of hemor¬ 
rhage within the cyst. 

The prognosis is generally good. 

The treatment is surgical. 


CANCER OF THE PANCREAS. 

Etiology.—The growth is more apt to occur in men than 
in women, and in those past thirty years of age. 

Pathology.— Cancer of the pancreas may be primary or 
secondary. Scirrhus is the most frequent variety. The 
growth may be limited to the pancreas or may spread to the 
stomach, the intestines, the peritoneum, or the liver. 

The symptoms are often obscure. Dyspeptic symptoms, 
loss of flesh and of strength, and cancerous cachexia are 
constant and progressive. When the head of the pancreas 
is involved (in one-third of all the cases) jaundice invariably 
results. Ascites results if the portal vein be pressed upon. 
The patient may at anytime vomit blood, from ulceration of 
the duodenum. The stools may be fatty; usually they contain 
undigested food. Glycosuria may be observed. Epigastric 
pain and tenderness are almost invariably present. A tumor 
is apparent in half the cases, and is of an irregular, more or 
less rounded form. The tumor is immovable, and may 
transmit a pulsation from the underlying aorta, so that 


CANCER OF THE PANCREAS. 


6l I 

in doubtful cases the patient should be examined in the 
knee-chest position. 

The duration of the disease is rarely over one year, and 
the result is invariably fatal. 

The treatment is entirely symptomatic. 


Of other varieties of new growths of the pancreas, sar¬ 
coma, cystic epithelioma , and syphiloma have been described, 
but they are all exceedingly rare. 


V. DISEASES OF THE KIDNEYS. 


CONGENITAL MALFORMATIONS OF THE 

KIDNEYS. 

There may be atrophy or congenital absence of one kid¬ 
ney, the other organ being considerably enlarged. Both 
kidneys may be fused into one horseshoe-shaped kidney, or 
into an irregular mass which may be displaced downward 
into the pelvis or either iliac fossa, or may lie in the middle 
line of the abdomen. These malformations must be remem¬ 
bered in operating on the kidney. Cases are on record in 
which calculi have been impacted in the ureter of a horse¬ 
shoe kidney, with complete anuria and death. 

MOVABLE KIDNEY. 

Synonyms— Floating kidney; Palpable kidney; Ren 
mobilis; Nephroptosis. 

The kidney is retained in place by its fatty capsule, by 
the peritoneum, and by the renal vessels. Under certain 
circumstances it becomes movable, pushing the peritoneum 
before it. In rare cases it may be invested with peritoneum, 
which is reflected at the hilum to form a mesonephron ; to 
such a condition the term “ floating kidney ” is limited by 
some. The right kidney alone is affected in 76 per cent, of 
all cases, both kidneys in 13 per cent., and the left kidney 
alone in 11 per cent. 

Etiology. —Congenital cases are rare. As an acquired dis¬ 
ease movable kidney is more common in women than in men, 
in the proportion of 9: 1. It is most common in multiparae, 
612 



MOVABLE KIDNEY. 


613 


in the laboring-classes, and after thirty-five years of age. It 
may be due to congenital laxity of the peritoneal attach¬ 
ments, to the laxity of the abdominal wall due to repeated 
pregnancies, to tight lacing, to severe bodily labor, or to 
absorption of the fatty capsule. The kidney may, moreover, 
be displaced downward by tumors. The term “ enterop- 
tosis ” has been applied to cases of prolapse of the abdomi¬ 
nal organs, especially of the transverse colon, with movable 
kidney, and frequently with dilatation of the stomach. 

Symptoms.—In the vast majority of cases there are no 
symptoms referable to the trouble, except that, should the 
tumor be accidentally discovered by the patient, nervous 
symptoms due to alarm and apprehension may result. In 
other cases there appear neurasthenic symptoms even to the 
verge of hysteria, with nervous indigestion, and in many 
instances accompanied by pain. This pain may be referred 
to the back, on the side of the movable kidney, and may 
radiate around the ribs, downward to the thigh, or forward 
to the epigastrium. The pain is aggravated or induced by 
exertion, jolting, or the erect posture. In some instances 
there may be merely a dragging feeling or a sense of weight 
or pressure. The pain may be the only symptom. 

In “floating kidney” there maybe, in rare instances, 
attacks characterized by intense abdominal pain, chills, 
vomiting, and symptoms of fever and collapse. The urine 
is usually diminished, high-colored, and contains an excess 
of uric acid or of oxalate of lime. These “ incarceration- 
symptoms ” are thought to be due to kinks or twists in the 
ureter or the renal vessels, but observations on this point 
are not definite. Care should be taken not to mistake these 
attacks for those of acute peritonitis, renal calculus, or 
appendicitis. Twisting of the ureter may give rise to tem¬ 
porary or permanent hydronephrosis, which may also be 
intermittent. Pyelitis may also result. A floating kidney 


6 14 MANUAL OF THE PFACTICE OF MEDICINE. 


may press on the bile-duct and cause jaundice, or on the 
vena cava and cause oedema of the legs. 

Physical Examination.—The patient being placed in the 
dorsal position with the knees drawn up and the abdominal 
wall relaxed, one hand is placed behind in the lumbar region 
while the other hand is placed in the hypochondrium under 
the margins of the ribs. Bimanual palpation reveals a solid 
smooth tumor, of the size and shape of the kidney, which 
is freely movable. It is not tender except on firm pressure. 
The detection of a movable kidney of the right side may be 
aided by asking the patient to take a long breath, so as to 
depress the liver and thus push the kidney down into reach. 
There is often an advantage in getting the patient to assume 
the knee-chest position. At times a number of examina¬ 
tions are requisite before a positive diagnosis can be made. 

Treatment is indicated only when the displacement of the 
kidney gives rise to symptoms. The simplest form of treat¬ 
ment is to put the patient in bed for a month and then let 
him go about with a binder and a pad to keep the kidney 
in place. This plan will work well in some cases, but not 
in others. In severe cases not relieved by this procedure 
surgical interference may be necessary, the kidney either 
being removed or being stitched in its proper place by 
sutures. 

ANOMALIES OP THE URINARY SECRETION. 

Albuminuria. 

Both serum-albumin and globulin can escape through 
the capillaries of the Malpighian tuft and appear in the urine. 
In practice it is not necessary to discriminate between these 
forms, and they are both commonly described by the term 
“albumin.” Albumin in the urine was formerly considered 
as a positive proof of organic disease of the kidney, but it is 


ANOMALIES OF THE URINARY SECRETION. 6I 5 


now known that not only may advanced nephritis exist 
without albumin, but that albumin may appear in cases 
without kidney-lesion, although in these cases it is supposed 
that there must be some failure in the nutrition of the epi¬ 
thelium of the capillaries of the tuft, allowing of the escape 
of albumin through them. Three distinct forms of albu¬ 
minuria are recognized : 

1. Spurious Albuminuria. —Urine admixed with blood (as 
in haematuria or in haemoglobinuria) or with pus will give 
the reaction for albumin in proportion to the amount of 
blood or of pus present. Tube-casts do not appear. 

2. Functional or Physiological Albuminuria. — (a) Albumin¬ 
uria may follow severe muscular exertion, sustained mental 
effort, excessive albuminous food, violent emotions, or cold 
bathing. A few hyaline casts may be present, especially 
after exertion. 

(b) Hcemic Causes. —Albuminuria may accompany any of 
the severe anaemias, purpura, scurvy, or syphilis. Under this 
heading may be included certain cases of transient albumin¬ 
uria occurring during pregnancy. 

(c) Abnormal Blood-ingredients , such as alcohol, bile- 
pigment, sugar, chronic lead- or mercury-poisoning, may 
induce the disease; it may also occur after the administra¬ 
tion of ether or chloroform. Hyaline casts also may be 
present in bile-stained urine. 

{d) Neurotic causes , probably from changes in the blood- 
supply, may give rise to the condition, as after epilepsy, apo¬ 
plexy, tetanus, or injuries to the head, and with exophthal¬ 
mic goitre. 

(e) Febrile albuminuria , with pyrexia from any cause, per¬ 
sisting during the period of fever. Albumin is present in 
small quantities, and is due to slight changes in the glom¬ 
eruli caused by the febrile process. 

if) Cyclic or periodic albuminuria is a form occurring in 


6 l6 MANUAL OF THE PRACTICE OF MEDICINE. 

young adults, especially in boys, in which albumin appears 
at certain times of the day. It seldom, if ever, occurs after 
rest at night, but usually after exertion or after the principal 
meal of the day. The quantity of albumin is usually small, 
although it may be considerable, and transient glycosuria or 
occasional hyaline casts may be present. 

In functional albuminuria there is neither high arterial 
tension nor hypertrophy of the left ventricle of the heart, 
unless from some intercurrent affection, and neither consti¬ 
tutional nor uraemic symptoms are present. Cases must 
always, however, be regarded with suspicion, especially if 
albumin be present in considerable quantities or if it be per¬ 
sistent. Albuminuria in persons over forty years of age 
usually indicates changes in the kidneys. 

3. Albuminuria with Gross Renal Lesions. — (a) Congestion 
of the kidney, either acute or chronic. 

( b ) Organic disease , acute and chronic nephritis, amyloid 
disease, and tumors. 

Tests.— The urine should be collected for twenty-four 
hours, and a specimen of this urine should be taken for 
examination. If the urine be turbid, it should be filtered, 
unless the turbidity be due to urates, in which case a little 
heat will clear the specimen. 

Heat-and-nitric-acid Test. —The urine is boiled in a test- 
tube. If opacity result, it is due either to albumin or to 
earthy phosphates. On adding a few drops of nitric acid the 
opacity disappears if due to phosphates; if due to albumin, 
it is permanent. This is the best routine test and the most 
satisfactory. 

Heller's Test. —Upon a small quantity of pure colorless 
nitric acid in a test-tube is allowed to trickle an equal 
amount of clear urine, so that it will overlie the acid. If 
albumin be present, a sharp white band will appear at the 
contact of the two liquids. A somewhat similar zone may 


ANOMALIES OF THE URINARY SECRETION. 617 

be formed by the action of nitric acid on urates if in excess, 
so that the more insoluble acid urates are precipitated. This 
zone, however, is not sharply defined, diffuses itself into the 
urine above, and disappears on the application of heat. A 
haze due to mucin may also occur above the albumin zone, 
and may obscure the test. 

Picnc-acid Test .—A saturated solution of picric acid may 
be used as in Heller’s test. Mucin, peptone, and certain alka¬ 
loids yield an opalescence with picric acid, but this opales¬ 
cence disappears on heating. 

Esbach s test is valuable in the quantitative analysis of 
albumin. The test-solution is made by dissolving io parts 
of picric acid and 20 parts of citric acid in 900 parts of 
boiling distilled water. After cooling, a sufficient quantity 
of distilled water is added to make a total of 1000 parts. 
The graduated tube is filled with urine to the mark U y and 
then with the reagent to the mark R. The liquids are 
mixed by slowly reversing the tube, and the coagulum of 
albumin is allowed to stand for twenty-four hours. The 
height of the sediment read on the etched scale indicates 
the weight of acid-albumin in grams per liter of urine. 

Other tests for albumin are superfluous, and for them the 
reader is referred to books on urinary analysis. 

Hematuria. 

Blood in the urine may come from the kidney, the pelvis 
of the kidney, the ureter, the bladder, or the urethra. 

Renal hemorrhage occurs after injuries or falls; after 
acute congestion or inflammation ; rarely from the atrophic 
form of chronic nephritis; from toxic agents, such as can- 
tharides, carbolic acid, and turpentine; from embolism, 
thrombosis, or aneurysm of the renal vessels; from tuber¬ 
cular inflammation; from new growths; from calculous 
pyelitis; with malignant forms of acute infectious fevers, as 


618 MANUAL OF THE PRACTICE OF MEDICINE. 


hemorrhagic small-pox or “ black measleswith certain 
hemorrhagic diseases, as scurvy, purpura haemorrhagica, or 
leukaemia; as evidence of vicarious menstruation; and in 
some young adults as a simple hemorrhage without known 
cause. It is also caused in the tropics by the parasites 
filaria sanguinis hominis and the Bilharzia. Malarial 
haematuria is endemic in certain of the Southern States. 

Hemorrhage from the ureter usually implies the passage 
of a calculus. 

Hemorrhage from the bladder is caused by injuries, rough 
catheterization, ulcers, ruptured veins, new growths, and 
calculi. 

Hemorrhage from the urethra is caused by traumatism, 
foreign bodies, calculi, ulcers, chancroids, rough catheteri¬ 
zation or injury, and gonorrhoea. 

Diagnosis.— Blood in the urine imparts to it a red or 
brownish color and gives the reaction for albumin. Haema¬ 
turia is to be distinguished from haemoglobinuria by the 
presence of red blood-corpuscles. Microscopical examina¬ 
tion usually renders other tests superfluous. 

Hellers test for blood-pigment consists in boiling the 
urine with a solution of caustic potash until flocculi of 
phosphates fall; these flocculi assume a red color from the 
freed haematin. 

The guaiacum test consists of the addition to the urine 
of a drop or two of tincture of guaiacum and two minims of 
ozonic ether. At the junction of the two fluids a blue line 
forms, which becomes diffused through the ether. Spectro¬ 
scopic examination may reveal the single band of reduced 
haemoglobin or the double band of oxyhaemoglobin. 

Care should be taken to exclude the admixture of men¬ 
strual blood from the specimen obtained for examination, 
and bloody urine should not be confounded with the stain¬ 
ing by rhubarb, logwood, and a few other dyes. 


ANOMALIES Of THE URINARY SECRETION. 619 


Determination of the Source of the Hemorrhage. —In 
blood from the kidney the blood and urine are intimately 
mixed, and there may be blood-casts, rendering the diag¬ 
nosis positive. The color is often smoky. Blood from the 
pelvis and the ureter is frequently passed in clots which 
resemble leeches in form and color. 

Blood from the bladder usually is passed with the last por¬ 
tion of urine. In washing out the bladder the water comes 
away blood-tinged, whereas if the source of hemorrhage 
were from the kidney the water would come away clear. 

Hemorrhage from the urethra occurs in the first part of 
micturition, and blood frequently escapes in the intervals. 
Local symptoms aid in revealing the source of the hemor¬ 
rhage. 

Hemoglobinuria. 

Whenever, from any cause, the red blood-corpuscles are 
dissolved in the blood, the coloring matter thus set free is 
excreted as methaemoglobin in the urine, imparting to it a 
reddish-brown color which may in extreme cases resemble 
that of porter. The urine contains granular pigment and is 
albuminous, but usually no red blood-corpuscles are pres¬ 
ent. If present, their number bears no proportion to the 
intensity of the color of the urine. 

Haemoglobinuria is to be distinguished from haematuria 
by the absence of red blood-corpuscles ; but care should be 
taken not to mistake haemoglobinuria for bloody urine in 
which the corpuscles have been dissolved during ammonia- 
cal decomposition. The urine reacts to Heller’s test (see 
page 618) and gives the spectroscopic absorption-bands of 
methaemoglobin or, more rarely, of oxyhaemoglobin. 

In all cases of haemoglobinuria that have terminated 
fatally a secondary nephritis has been found. 

Two clinical groups of haemoglobinuria are described : 

I. Toxic Hemoglobinuria .—Dissolution of the red blood- 


620 MANUAL OF THE PRACTICE OF MEDICINE . 


corpuscles can occur from the ingestion of certain drugs, 
such as potassium chlorate, carbolic acid, pyrogallic acid, 
naphthol, chloral, arseniuretted hydrogen, and muscarine. 
Haemoglobinuria occurs after transfusion of blood, especially 
the blood of animals into the human subject, and after exten¬ 
sive superficial burns ; it is said also to occur after exposure 
to cold. It may occur with certain infectious diseases, such 
as typhoid fever, scarlet fever, malarial fever, yellow fever, 
and syphilis, and an epidemic form of haemoglobinuria in 
the new-born has been described, characterized by jaundice, 
cyanosis, and nervous symptoms. 

2. Paroxysmal Hemoglobinuria .—This form is character¬ 
ized by the passage of blood-pigment in the urine in 
attacks. It is more common in men than in women, and it 
is usually seen in adults. Attacks may be induced by 
exposure to cold or as the result of bodily or mental 
exhaustion. Patients suffering from Raynaud’s disease are 
peculiarly susceptible. Severe malarial poisoning may 
cause either haematuria or haemoglobinuria, the changes in 
the urine frequently showing some regular periodicity. 
The attacks may be preceded by a chill and a rise in tem¬ 
perature, or the temperature may be subnormal. There 
may be yawning, headache, pain in the bones, vomiting, 
and cramp-like pains over the hepatic or lumbar region. 
The haemoglobinuria rarely persists for more than one day; 
it then subsides, and is followed by slight jaundice in a 
considerable number of cases. Urticaria after the paroxysm 
is not uncommon. Ralfe describes cases in which parox¬ 
ysms of haemoglobinuria alternate with the same general 
symptoms, but with the passage of albumin and an in¬ 
creased amount of urea. 

The prognosis of the toxic form of haemoglobinuria 
depends upon the severity of the primary disease; other¬ 
wise the prognosis is good. 


ANOMALIES OF THE URINARY SECRETION. 621 


Treatment is unsatisfactory. Exposure to cold should 
be avoided ; quinine should be given in malarial cases, and 
iodide of potassium is to be administered should a syphilitic 
history be obtained. During the paroxysm the patient 
should be confined to bed, kept warm, and given hot 
drinks. 

Pyuria (Pus in the Urine). 

Etiology.— i. Pyelitis and Pyelonephritis. —The pus is 
uniformly mingled with the urine, and the condition of the 
urine is unchanged after the bladder has been washed out. 
In calculous and tubercular pyelitis the urine is usually acid 
in reaction, but in pyelitis complicating cystitis the reaction 
is usually alkaline. Large abscesses of the kidney may 
suddenly discharge a large quantity of pus, and for days or 
weeks afterward the urine may be free. 

2. Cystitis. —The urine is alkaline, often ammoniacal. 
The pus is passed with the last portions of the urine, and 
is mixed with thick, ropy mucus. The urine first obtained 
after the bladder has been washed out shows decided im¬ 
provement. 

3. Urethritis. —The pus is passed with the first portion 
of the urine, and may escape from the meatus in the intervals 
of micturition. Local symptoms of inflammation are usually 
evident. 

4. Leucorrhcea. —The pus is small in quantity and is ad¬ 
mixed with vaginal epithelium. This condition may be 
excluded by ordering a vaginal douche to be given before 
micturition, and by the use of the catheter. 

5. Rupture of an abscess into the urinary passages is 
characterized by a sudden irruption of pus. 

Peptonuria. 

Peptone is never found in healthy urine. Traces of it 
are found in some acute diseases, in suppurative processes, 


622 MANUAL OF THE PRACTICE OF MEDICINE. 

and with disturbances of the digestion of albuminous sub¬ 
stances, but the peptonuria possesses no diagnostic value. 

Tests .—Peptone is not precipitated by heat or by nitric 
acid, but with picric acid there occurs a precipitate which 
is dissolved by heat. A supernatant layer of urine over 
Fehling’s solution yields a rose-pink halo. 

Phosphaturia. 

Phosphates occur in the urine as alkaline salts of sodium 
and potassium and as earthy salts of lime and magnesium. 
In urine undergoing ammoniacal fermentation the am- 
monio-magnesium salt or the triple phosphates may appear. 

Phosphates are soluble only in neutral or acid urine, and 
are precipitated whenever the urine becomes alkaline. As 
they are less soluble in hot solutions, the phosphates are 
often precipitated by boiling, even in urine of a slightly acid 
reaction, and may be mistaken for albumin; but the speci¬ 
men rapidly clears up upon the addition of acetic acid. If 
this acid be added to the specimen before boiling, precipi¬ 
tation does not occur. 

Phosphates may appear in excess (up to y to g grams, 
whereas from 2 to 3 grams is the normal quantity) in those 
suffering from debility, dyspepsia, or wasting disease. There 
has been described a phosphatic diabetes characterized by 
polyuria, thirst, loss of flesh, and an absence of sugar in the 
urine. In some cases glycosuria or diabetes has followed 
this condition. 

Lith^emia; UriCjEmia. 

The daily amount of uric acid excreted depends largely 
upon the diet, varying from 10 to 30 grains, the relation of 
uric acid to urea being normally as 1 : 33. As to the pro¬ 
duction and antecedents of uric acid not much is known 
accurately, although it is supposed to be formed in the liver 
ft om ammonia and lactic acid. It is also unknown whether 


ANOMALIES OF THE URINARY SECRETION 623 

it represents a suboxidized grade of urea or whether it has 
an independent origin. Uric acid, being practically insolu¬ 
ble, is eliminated by the kidneys chiefly as the urates of 
sodium and ammonium, and to a less extent as the urates 
of potassium, calcium, and lithium. From these bases uric 
acid may be separated, forming the “ red-pepper ” or 

brick-dust deposits, which show characteristic appear¬ 
ances under the microscope. As conditions which cause 
the precipitation of uric-acid crystals from the urine 
Roberts mentions—(1) High acidity; (2) poverty in min¬ 
eral salts; (3) low pigmentation; and (4) high percentage 
of uric acid. More commonly occurs the precipitation of 
amorphous urates, chiefly as the acid sodium urate, in the 
form of a pinkish deposit occurring as the urine cools. The 
urine is usually concentrated, of high specific gravity, and 
of excessively acid reaction. 

The power which the blood possesses of holding uric 
acid in solution depends upon its degree of alkalinity. 
According to Haig, the excretion or the retention of uric 
acid can be regulated by increasing or diminishing the alka¬ 
linity of the blood. His theory is that agents increasing 
the alkalinity, finding a considerable quantity of uric acid 
in the liver, the spleen, and the tissues, render its solubility 
more perfect, so that it is taken into the blood and excreted 
by the kidneys. Pre-eminent among the drugs that increase 
the elimination of uric acid is sodium salicylate. Among 
those drugs causing retention, the most important are acids. 
Haig further believes that drugs affect only the excretion 
of uric acid, and have no influence whatever upon its 
formation. 

The term “ lithaemia ” was first used by Murchison to 
designate symptoms due to functional disturbance of the 
liver and accompanied by an increased elimination of uric 
acid or urates; but it is impossible, in the present state of 


624 MANUAL OF THE PRACTICE OF MEDICINE . 


our knowledge, to state with any accuracy the pathology 
of the uric-acid diathesis. The diathesis bears a close 
relationship to gout, so that it has been termed “ Amer¬ 
ican gout.” For its etiology and symptomatology see 
Irregular Gout. 


OXALURIA. 

Oxalate of lime is held in solution in the urine by the 
acid sodium phosphate. The crystals, which may be found 
deposited in small quantities under certain conditions, are 
easily recognized under the microscope. Oxaluria occurs 
after eating certain fruits and vegetables, as tomatoes, 
rhubarb, apples, pears, and cauliflower. It occurs also in 
gouty, hypochondriacal, and neurasthenic patients, as the 
result of imperfect oxidation-processes. Oxaluria is also 
said to result from acid fermentation of the urine within the 
urinary passages. 

Chyluria. 

Rare cases of chyluria result from some connection 
between the lymphatic vessels and the urinary passages, but 
the exact pathology is unknown. In the tropics chyluria 
is not infrequently associated with the presence of the filaria 
sanguinis hominis. The urine is milky in appearance and 
contains emulsified fat and serum-albumin. There may 
occur a spontaneous clot resembling blanc-mange, or the 
fat-globules may rise to the surface like cream. The 
microscope shows fine fat-globules which dissolve in ether. 

Indicanuria. 

Indigo appears in the urine, not in the free state, but in 
combination as indoxyl-sulphate of potassium, which is a 
compound originally derived from indol. Indol itself is 
formed in the small intestine by the action of bacteria upon 


ACUTE CONGESTION OF TIIE KIDNEYS. 6 25 

albumin. When concentrated acids are added to the urine 
containing the indoxyl-sulphate, indigo is liberated. 

Indicanuria is frequent in all wasting and cachectic 
diseases associated with the excessive destruction of albu¬ 
minoids. It may occur with tumors of the intestines and 
the pancreas, in intestinal obstruction, and in prolonged 
constipation. It is increased by a milk diet. 

Glycosuria. 

It is a generally accepted belief that sugar does not occur 
in normal urine. The occurrence of glycosuria with patho¬ 
logical conditions will be considered elsewhere, under the 
same heading. 

Lipuria. 

Fat may appear in the urine after an excessive quantity 
of fat has been taken with the food, with prolonged sup¬ 
puration, with pancreatic tumors and degeneration, after 
phosphoi us-poisoning, and in diabetic urine. The occur¬ 
rence of chyluria has already been described. Lipuria may 
also occur with advanced Bright’s disease and with pyo¬ 
nephrosis. 

Acetonuria. 

Acetone, according to Von Jaksch, may occur with fevers, 
diabetes, cancer, inanition, in certain mental conditions, and 
as a form of auto-intoxication. 

For the clinical and microscopical detection of the above- 
mentioned ingredients of the urine the reader is referred to 
books on urinary analysis. 

ACUTE CONGESTION OF THE KIDNEYS. 

Etiology. Acute congestion of the kidneys may follow 
the taking of certain poisons (as cantharides), the removal of 

one kidney, or the sudden blocking of one ureter by a cal- 
40 


626 MANUAL OF THE PRACTICE OF MEDICINE . 

cuius, by over-exertion, or by surgical operations, especially 
on the bladder and the urethra. 

Pathology. —The lesion consists in the temporary con¬ 
gestion of the blood-vessels of the kidney, allowing of the 
exudation of serum and the escape of red blood-cells. 

Symptoms. —The urine, which is diminished in quantity 
or suppressed, according to the degree of congestion, may 
contain blood, albumin, and casts. Its specific gravity is 
not changed. The urinary symptoms may last for a few 
days with considerable prostration, and may then disappear; 
or the symptoms may continue, and the patient becomes 
more feeble and prostrated, passes into a typhoid state with 
delirium, and dies. These bad cases are those following the 
removal of one kidney, impaction of a calculus, or surgical 
operations on the bladder and the urethra. 

The prognosis in mild cases is good. Repeated attacks 
induced by over-exertion or by irritant drugs may event¬ 
ually lead to nephritis. 

Treatment. —The patient is to be kept warm in bed, on a 
liquid diet, and the bowels are to be moved freely. Sweat¬ 
ing should be induced by pilocarpine or by the hot pack or 
the hot-air bath. 

CHRONIC CONGESTION OF THE KIDNEYS. 

Etiology and Synonym. —Chronic congestion of the 
kidneys is induced by any cause preventing the free escape 
of blood from the renal veins, such as the pressure of ab¬ 
dominal growths or that occurring in the course of chronic 
congestion of the viscera due to heart disease or to emphy¬ 
sema. Synonym: Cyanotic induration. 

Pathology. —The kidneys are normal or increased in size 
and are heavy and hard. The capsule is not adherent; the 
surface is smooth. The organ is congested, red, and livid, 
or the pyramids are red while the cortex is pink or white. 


ACUTE DEGENERATION OF THE KIDNEYS. 627 

A considerable number of the glomeruli are large, their capil¬ 
laries are dilated, and the cells covering the capillaries are 
swollen. Aside from a slight increase in the subcapsular 
connective tissue, the stroma is unchanged. Such kidneys 
are apt to develop chronic diffuse nephritis. In heart dis¬ 
ease with visceral congestions chronic diffuse nephritis 
occurs in 60 per cent., chronic congestion in 40 per cent. 

Symptoms. —The urine is diminished in quantity but is 
of good quality, the amount of urea to the ounce being- 

o 

rather increased than diminished. The specific gravity is 
normal or high. Albumin and casts may be present in 
small quantities, but are often absent. A continual precipi¬ 
tation of urates should excite suspicion of chronic conges¬ 
tion, and the heart and lungs should be carefully examined. 
The general symptoms are slight or unnoticed. Ursemic 
symptoms do not occur. 

Treatment should be directed toward the disease causing- 
the congestion. 

ACUTE DEGENERATION OP THE KIDNEYS. 

Etiology and Synonyms. —Acute degeneration of the 
kidneys is always secondary to the introduction of poisons 
into the body. It complicates poisoning by arsenic, mer¬ 
cury, and phosphorus, or by the organic poisons which 
result from severe infectious diseases or from injuries. 
Acute degeneration is usually found in the kidneys of 
those who have died from infectious diseases. Synonyms: 
Acute Bright’s disease; Parenchymatous nephritis; Paren¬ 
chymatous degeneration. 

Pathology. —The kidneys are more or less enlarged ; 
the capsules are not adherent; the surfaces are smooth; the 
cortex is usually thickened, and it may be either pale or con¬ 
gested. There are changes in the renal cells, especially 
marked in those of the convoluted tubes. These changes 


628 MANUAL OF THE PRACTICE OF MEDICINE. 

consist in (i) swelling, (2) granular infiltration with albumi¬ 
noid matter and fat, (3) death of the cells, with desquama¬ 
tion, (4) a formation of hyaline masses in the cells, and (5) 
a growth of new cells to replace the dead epithelium. In 
severe cases there is added congestion of the blood-vessels, 
with exudation of serum. There are no changes in the 
stroma. 

Symptoms. —The urine is diminished according to the 
severity of the disease. It may even be suppressed. Its 
specific gravity is unchanged. Albumin and casts are usually 
present, from the congestion and exudation, and blood-cells 
appear in severe cases. The general symptoms are usually 
obscured by those of the primary disease. In mild cases 
accompanying infectious diseases there are no symptoms, 
excepting the presence of albumin and casts in small amounts 
in the urine. In severe cases accompanying yellow fever 
and acute yellow atrophy of the liver, and following the 
ingestion of an inorganic poison, the urinary changes are 
marked : the patient becomes feeble, passes into the typhoid 
condition, and dies, apparently from the kidney-lesion. 
Dropsy is not noticeable in these cases. 

The prognosis is good except in the severe cases. Albu¬ 
min and casts may, however, persist for some time after the 
subsidence of the primary disease. 

Treatment. —There is no treatment to prevent the degen¬ 
erative changes. When exudation occurs the treatment of 
acute exudative nephritis is indicated. 

CHRONIC DEGENERATION OF THE KIDNEYS. 

Etiology and Synonyms. —The process is secondary to 
any of the mechanical causes of chronic congestion, to 
vicious modes of life, and to chronic alcoholism. Synonyms: 
Chronic Bright’s disease; Chronic parenchymatous nephri¬ 
tis; Fatty kidney. 


ACUTE EXUDATIVE NEPHRITIS. 629 

Pathology. —The kidneys are usually increased in size, 
although exceptionally they may be normal or even small. 
The surface is smooth; the pyramids are red; the cortex is 
white, yellow, or pink. There are swelling, granular degen¬ 
eration, and fatty infiltration of the epithelium of the cortex. 
There are no changes in the stroma. The glomeruli are 
normal unless the degeneration be due to venous congestion. 

Symptoms. —The quantity ol urine varies in different 
patients and at different times; it may be increased, normal, 
scanty, or the urine may be suppressed. The specific grav¬ 
ity of the urine and the proportion of urea excreted are 
unchanged. Albumin and casts in moderate amounts are 
usually present. The patient becomes anaemic and loses 
flesh and strength. In bad cases he may pass into the 
typhoid state, with delirium and stupor. Dropsy does not 
develop. The disease may be followed by chronic nephritis. 

The prognosis is not good, as the natural tendency of 
the disease is to progress. 

Treatment is not satisfactory. Vicious and alcoholic 
habits are to be checked. The diet and the mode of life 
are to be regulated. The circulatory changes inducing 
venous congestion are to receive appropriate treatment. 

ACUTE EXUDATIVE NEPHRITIS. 

Etiology and Synonyms. — Primary cases may occur 
after exposure to wet and cold, or without assignable cause. 
Secondary cases accompany any of the severe infectious dis¬ 
eases or the puerperal state. Synonyms: Parenchymatous 
nephritis; Tubal nephritis; Desquamative nephritis; Ca¬ 
tarrhal nephritis; Croupous nephritis; Glomerulo-nephritis. 

Pathology. —The chief lesion is in the blood-vessels. 
From the tuft there is an exudation of plasma and of 
red and white blood-cells which infiltrate the stroma of the 
kidney and collect as casts and cellular masses in the tubes, 


630 MANUAL OF THE PRACTICE OF MEDICINE. 

from which they may be voided in the urine. The amount 
of exudation varies with the severity of the case. In severe 
cases there may be an over-production of pus-cells. 

In mild cases the kidney shows no changes, the conges¬ 
tion having disappeared and the exuded material having 
been passed in the urine. 

In severe cases the kidney is large, the surface is smooth, 
the cortex is thick and white or red and white, or the whole 
kidney is congested and succulent. Within the tubes, espe¬ 
cially those of the cortex, are irregular masses of coagulated 
material, forming casts, and frequently white and red blood- 
cells. There may be dilatation of the cortical tubes, and their 
epithelium may be swollen, degenerated, or detached. The 
cells covering the tuft are usually swollen and increased in 
number. In other cases there is an excessive emigration 
of white blood-cells, which infiltrate the stroma and appear 
as small whitish foci in the cortex. The amount of serum 
exuded from the tuft is not proportionately increased, so 
that it is possible in this form to have little or no albumin 
and casts in the urine. 

Symptoms. —In mild cases the patient complains of gen¬ 
eral malaise, with slight headache, loss of appetite, and per¬ 
haps some aching in the back. The urine is slightly dimin¬ 
ished in quantity, the specific gravity is about normal, and 
albumin is present in considerable quantity, with hyaline, 
granular, and epithelial casts, sometimes with red and white 
blood-cells. The constitutional symptoms last for from 
one to two weeks ; albumin and casts persist for four or six 
weeks and then disappear. 

In severe cases there is fever, with prostration, loss of 
appetite, nausea, a pulse of high tension, and exaggerated 
heart-action. Anaemia is rapidly developed. There may 
appear the symptoms of acute uraemia due to contracted 
arteries—stupor, headache, dyspnoea, restlessness, muscular 


ACUTE EXUDATIVE NEPHRITIS. 


631 

twitchings, or general convulsions. Dropsy may be de¬ 
veloped, usually appearing first in the face. The urine is 
diminished in quantity, and contains albumin, casts, and 
cells in proportion to the severity of the inflammation. 
Constitutional symptoms last about four weeks. Albumin 
and casts continue in the urine for weeks afterward. 

The cases with abundant production of pus-cells occur in 
children and in adults as a primary disease or secondary 
to measles, scarlet fever, and diphtheria. The invasion is 
sudden, with fever and prostration. Restlessness, delirium, 
headache, and stupor appear early in the disease and con¬ 
tinue throughout its course. Dropsy is slight or absent. 
The patient loses flesh and strength, passes into the typhoid 
condition, and is apt to die. 

The urine is not much diminished in quantity; its specific 
gravity is normal. Albumin, casts, and red and white 
blood-cells are usually present in considerable quantity, but 
they may not appear until late in the disease. In other 
cases albumin and casts are scanty or are absent altogether. 

The prognosis of mild cases is good. The development 
of ursemic symptoms in the severe cases causes anxiety, but 
a decided majority of the cases recover completely. The 
cases with abundant production of pus-cells are apt to 
terminate fatally. It is possible for the disease to be fol¬ 
lowed by chronic nephritis. 

Treatment. —The patient should be put to bed on a milk 
diet. In mild cases the liberty of the house may be allowed. 
The bowels should be kept open by calomel or by sulphate 
of magnesium in small repeated doses, and the skin should 
be rendered active by hot baths, daily cleansing, and skin- 
friction. Applications of wet or dry cups or hot poultices 
to the lumbar region may be of service. The cerebral 
symptoms during the early part of the disease, being due to 
contraction of the arteries with labored heart-action, should 


632 MANUAL OF THE PRACTICE OF MEDICINE. 

be controlled by arterial dilators. Of these, the best are 
aconite, chloral hydrate, nitroglycerin, and opium, in small 
repeated doses before the cerebral symptoms are marked, and 
in larger doses, hypodermically and by the rectum, during an 
attack. As the nephritis subsides the milk diet is replaced 
by solid food, iron and oxygen are given for the anaemia, and, 
if possible, the patient is sent to a warm, dry inland place 
until convalescence is complete. 

ACUTE DIFFUSE NEPHRITIS. 

Etiology and Synonyms. —Primary cases of acute diffuse 
nephritis follow exposure to wet and cold. Secondary cases 
complicate scarlet fever, diphtheria, and pregnancy. The 
disease is more common in children and young adults. 
S ynonyms: Acute productive nephritis; Acute Bright’s 
disease; Croupous nephritis. 

Pathology. —The kidneys are large; the capsule is not 
adherent unless in cases of old standing, in which event the 
surface may also be roughened; the cortex is thick, white, 
mottled yellow and red, or congested; the pyramids are 
red. The microscope shows the same lesions as in acute 
exudative nephritis, with two additional features : First, a 
growth of connective tissue in the cortex; second, a growth 
of the capsule-cells of the Malpighian tufts. These changes 
do not occur throughout the entire kidney, but in symmet¬ 
rical wedges in the cortex, following the line of the arteries. 
These wedges may be small or large, few or numerous, reg¬ 
ular or irregular. Each wedge has the same general 
characters : 

First, one or more arteries which run toward the cortex, 
the walls of which are thickened. 

Second, the Malpighian bodies connected with the affected 
artery show an increased growth of capsule-cells, causing 
compression of the tufts. There is also a growth of the cells 


ACUTE DIFFUSE NEPHRITIS. 


633 


covering the vessels and within them, as in exudative nephri¬ 
tis. The tuft never returns to a normal condition, but in 
time the vessels are obliterated and the glomeruli are 
transformed into little balls of fibrous tissue. 

Third, a growth of connective tissue in the stroma paral¬ 
lel with the affected arteries. This connective tissue is at 
first composed largely of cells; later the tissue becomes 
denser. If the growth of connective tissue be abundant, 
the tubes within the wedge become atrophied. 

Between the wedges are seen the lesions of exudative 
nephritis; later there is developed a diffused growth of 
connective tissue. 

The disease is serious not only from the disturbed func¬ 
tions of the kidney induced, but also because of the perma¬ 
nent character of the lesion. 

Symptoms.—The invasion may be sudden or gradual. 

The acute cases begin with fever and prostration, pain in 
the back, and frequent, scanty micturition. There are 
symptoms of acute uraemia, a pulse of high tension with 
exaggerated heart-action, or hypertrophy of the left ven¬ 
tricle, loss of appetite, nausea or vomiting, stupor, headache, 
muscular twitchings, or even convulsions. The patient be¬ 
comes rapidly anaemic, and dropsy appears, usually first in 
the face; the dropsy may become general. The urine is 
smoky or bloody in color, scanty or even suppressed, of a 
low specific gravity, and contains albumin and casts in con¬ 
siderable quantities, with renal epithelium, and sometimes 
with pus-cells. These acute cases resemble cases of acute 
exudative nephritis, but the specific gravity of the urine is 
lower and the patient is more apt to die. At the end of 
about four weeks, however, the patient may apparently re¬ 
cover, although albumin and casts still persist in the urine. 
In course of time symptoms of chronic nephritis appear. 

The subacute cases are more frequent. The first symp- 


634 MANUAL OF THE PRACTICE OF MEDICINE. 


toms are often referred to the stomach—loss of appetite, 
nausea, and vomiting. In other patients dropsy is the first 
symptom complained of. Anaemia, headache, sleepless¬ 
ness, and dyspnoea usually appear early in the disease. The 
urine is diminished in quantity, is of a low specific gravity, 
and may or may not contain blood. Albumin and casts 
are present, the former usually in considerable quantity. 
The patient becomes gradually worse. Acute uraemia 
from contracted arteries is shown by high-tension pulse, 
exaggerated heart-action or hypertrophy, with or without 
some dilatation of the left ventricle, headache, restlessness, 
and muscular twitchings or convulsions. Chronic uraemia 
is shown by alternating delirium and stupor, with a feebly 
acting heart and low arterial tension. The attack may last 
for weeks or months, and from it the patient may die. 
Other patients apparently recover, but the urine still con¬ 
tains albumin and casts and is of low specific gravity. 
There are usually subsequent attacks, which must be re¬ 
garded as acute exacerbations of an established chronic 
nephritis. 

The prognosis is bad, the patient dying either in the 
acute attack or from the chronic nephritis that follows. In 
many cases life may be prolonged for a number of years. 

Treatment.—In the acute cases the treatment is the 
same as that for exudative nephritis, except that more 
care should be employed during convalescence, and pro¬ 
longed residence in a warm inland climate should be 
recommended. 

In the subacute cases the nephritis is best treated by rest 
in bed on a milk diet. The milk diet should be continued 
for a few weeks, and should then gradually be replaced by 
solid food. Later, residence in a warm, dry climate for 
some months at least should be insisted upon. Anaemia is 
to be treated by iron, oxygen, and fresh air. The dropsy 


CHRONIC BRIGHT'S DISEASE. 


635 


is best treated by rest in bed on a milk diet. If the dropsy 
be persistent, diuretics, cathartics, and the hot pack or the 
hot-air bath may be employed. The condition of the heart 
and the arteries should be watched continually. If the 
arteries be contracted, with a pulse of high tension and an 
exa gg e rated heart-action, arterial dilators should be used. 
Among the best of these are nitroglycerin, chloral hydrate, 
opium, and potassium iodide. If the heart be feeble, with 
low-tension pulse, and if symptoms of chronic uraemia appear, 
digitalis, strophanthus, caffeine, or strychnine is indicated. 
In all cases the patient should be watched during convales¬ 
cence, and the general health should be improved in every 
possible way. The selection of a suitable warm climate is 
of the very first importance in these cases. 

CHRONIC BRIGHT’S DISEASE. 

Although two forms of chronic nephritis are described, 
one with and one without exudation from the blood-vessels, 
practically the same lesions are found in both. The only 
real difference is that in one form exudation from the vessels 
is added. In chronic nephritis with exudation albumin is 
nearly constantly present in the urine, although it may be 
absent for short periods. In chronic nephritis without 
exudation albumin is generally absent, although it may be 
present at times in considerable quantity. The presence or 
absence of albumin seems to vary the clinical symptoms of 
the disease to some extent. 

Chronic Diffuse Nephritis with Exudation. 

Etiology and Synonyms. —Primary cases occur in young 
and middle-aged adults, being somewhat more common in 
males. The disease may follow acute diffuse nephritis, 
whether from cold, scarlet fever, or pregnancy, and it occurs 
after chronic congestion and chronic degeneration of the 


636 MANUAL OF THE PRACTICE OF MEDICINE. 


kidney. It may complicate syphilis, endocarditis, chronic 
phthisis, and prolonged suppuration, especially of bones 
and joints, and it is usually associated with amyloid degen¬ 
eration of the kidney. Synonyms: Chronic parenchyma¬ 
tous nephritis; Large white kidney; Small white kidney; 
Chronic desquamative nephritis; Chronic tubal nephritis. 

Pathology. —The kidneys are usually large, with smooth 
or roughened surfaces ; the cortex is pale. This condition 
is spoken of as the “ large white kidney.” In other cases 
the kidney is small, with a pale cortex, forming the “ small 
white kidney.” In rare cases the kidney may appear to the 
eye to be normal. Microscopically the following changes 
are described by Delafield : “There is a very extensive 
growth of connective tissue in the cortex ; the renal epithe¬ 
lium is swollen, granular, degenerated, fatty, broken, or flat¬ 
tened ; the tubes contain coagulated matter, cast matter, or 
blood ; the cortex-tubes are atrophied in some places, dilated 
in others. 

“ The glomeruli are changed in several different ways : 

“ 1. There is a growth of the capsule-cells in such num¬ 
bers that they.compress the tufts. The cells covering the 
capillaries are also increased in size and number. The 
capsule-cells may finally be changed into connective tissue, 
and the tufts become atrophied. 

“ 2. The glomeruli are of large size; the cells covering 
the capillaries are increased in number, so that the outlines 
of the capillaries are lost, but yet the capillaries are not 
compressed nor are the glomeruli atrophied. 

“ 3. There is a growth of the cells which cover the capil¬ 
laries and of the cells within them. Of the cells which cover 
the capillaries, the cell-bodies become very large, the capil¬ 
laries are compressed, and the glomeruli eventually become 
atrophied. 

“ 4. The walls of the capillary vessels become the seat 


CHRONIC BRIGHTS BISEA SR. 637 

of waxy degeneration, while the cells which cover them are 
increased in size and number. 

‘‘5. If the nephritis follows chronic congestion, the capil¬ 
laries are dilated, and there is an increase in the size and 
number of the cells which cover the capillaries. 

“ The arteries remain unchanged, or they are the seat of 
obliterating endarteritis, or there is a symmetrical thicken¬ 
ing of all the coats of the artery, or all the coats of the artery 
are thickened and converted into a uniform mass of connec¬ 
tive tissue, or there is waxy degeneration of the walls of the 
arterv.” 

Symptoms.— 1. Changes in the Urine .—The quantity 
varies at different times. When the inflammation is quies¬ 
cent the quantity may be normal; during an acute exacer¬ 
bation the urine is diminished or suppressed. In some 
cases, when the patient is doing badly, even if there be 
dropsy, the urine is increased. The specific gravity and 
the amount of urea to the ounce slowly diminish. The 
gravity varies usually between 1001 and 1012. Low specific 
gravity indicates extensive connective-tissue growth in the 
cortex or waxy degeneration of the capillaries of the glo¬ 
meruli. Albumin and casts are almost constant in con¬ 
siderable quantities; they are increased during acute ex¬ 
acerbations, and at other times, when the lesion is quiescent, 
they may diminish, and may even disappear for short 
periods. 

2. Dropsy is a prominent symptom, and is rarely absent. 
It may occur early or late, or only in periods. 

3. Anosmia is most marked, and may even resemble per¬ 
nicious anaemia. There is a peculiar pallor of the skin 
which is quite characteristic. 

4. Acute urezmic symptoms, with contracted arteries, caus¬ 
ing convulsions, etc., are not as common as in the cases 
without exudation. 


638 MANUAL OF THE PRACTICE OF MEDICINE. 

5. Chronic anemia , with soft, feeble pulse, delirium, and 
stupor, is common, especially toward the close of the 
disease. 

6. Headache, restlessness and sleeplessness, loss of appe¬ 
tite, nausea, and vomiting frequently occur. 

7. Neuro-retinitis and nephritic retinitis are not as common 
as in the cases without exudation. 

8. Dyspnoea is nearly constant. It may be due to hydro¬ 
thorax, to oedema of the lungs, to failure of the heart, or to 
contraction of the arteries. In many cases spasmodic 
dyspnoea occurring at night or in the early morning, and 
aggravated by lying down, may be the first symptom 
noticed. 

9. The tension of the pulse is usually, but not always, in¬ 
creased. There may be hypertrophy or dilatation of the 
left ventricle, myocarditis, or feeble heart. 

Course of the Disease. —The constant symptoms are 
(1) albumin in the urine, (2) dropsy, and (3) anaemia. 

1. In some cases the symptoms are continuous, the patient 
dying from chronic uraemia or dropsy in from one to two 
years. 

2. The symptoms come in attacks. Between the attacks 
the patient feels well, although the urine contains albumin 
and is usually of low specific gravity. The interval between 
the attacks may be weeks, months, or even years. 

3. Some patients live for years with only pallor of the 
skin and albumin in the urine, feeling well otherwise. 

4. There may be an attack of spasmodic dyspnoea in a 
time of supposed good health. Years may intervene before 
symptoms are developed. 

5. There may be a history of chronic endocarditis, con¬ 
gestion of the kidney, or acute diffuse nephritis before the 
regular symptoms of the disease appear. 

6. A few cases apparently recover, especially in children. 


CHRONIC BRIGHT'S DISEASE. 639 

The prognosis is bad, although life may be prolonged 
for years. 

Tieatment. The amount of urine should be increased 
by drugs or by so regulating the diet of food and liquids 
that the patient passes sixty ounces of urine a day. 

The dropsy is to be treated by rest in bed, diuretics, and 
cathartics. Arterial dilators or heart-stimulants are indicated 
to meet the respective errors in the circulatory system. 

Anaemia requires iron, arsenic, and oxygen. Prolonged 
residence, especially during the winter months, in a warm, 
dry climate is of great importance. 

Acute uraemia with contracted arteries requires arterial 
dilators, such as nitroglycerin, chloral hydrate, opium, and 
potassium iodide, or bloodletting. 

In chronic uraemia, with delirium, stupor, and a feeble 
heart, we employ the hot pack, heart-stimulants, and cathar¬ 
tics, but the results are not usually satisfactory. 

During the acute exacerbation the patient should be put 
to bed on a milk diet and treated as if he had acute nephritis. 
Between the exacerbations plenty of outdoor life in fresh 
warm air may be advised, but not to the point of fatigue. 

Chronic Diffuse Nephritis without Exudation. 

Etiology and Synonyms.—This disease usually occurs 
in those over twenty years of age. It may appear in adults 
in a primary form as a gradual degeneration of the kidney; 
it often runs in families having a tendency to degeneration 
of the arteries. It may be caused by chronic alcoholism, 
lead-poisoning, gout, excessive eating and drinking, lithae- 
mia, and constitutional syphilis. These causes are also 
factors in causing emphysema, endocarditis, endarteritis, 
and cirrhosis of the liver, with which diseases the nephritis 
is often associated. This form of nephritis also follows 


640 MANUAL OF THE PRACTICE OF MEDICINE. 

chronic congestion of the kidney, hydronephrosis, and 
chronic pyelitis. Synonyms: Chronic interstitial nephritis ; 
Cirrhosis of the kidney; Granular kidney; Atrophic form 
of chronic diffuse nephritis; Gouty kidney; Renal sclero¬ 
sis ; Arterio-sclerotic kidney. 

Pathology.—The kidneys are diminished in size; the 
capsules are adherent; the surfaces are granular ; the cortex 
is thinned and of a red or gray color. There may be small 
cysts on the surface. Rarely the kidney is normal or even 
increased in size. The following microscopical changes are 
described by Delafield : “ There is a growth of new connec¬ 
tive tissue in the cortex, and also in the pyramids, which 
becomes more and more marked as the disease goes on. 
In the cortex the new tissue follows the distribution of the 
normal subcapsular areas of connective tissue, is in the form 
of irregular masses, or is distributed diffusely between the 
tubes. In the pyramids the growth of new connective tissue 
is diffuse. The tubes, both in the cortex and in the pyra¬ 
mids, undergo marked changes. Those included in the 
masses of connective tissue are diminished in size; their 
epithelium is flattened; some contain cast matter, many are 
obliterated. The tubes between the masses of new connec¬ 
tive tissue are more or less dilated; their epithelium is flat¬ 
tened, cuboidal, swollen, degenerated, or fatty. The dilata¬ 
tion of the tubes may reach such a point as to form cysts 
of some size which contain fluid or coagulated matter. 
These cysts follow the lines of groups of tubes or are situ¬ 
ated near the capsules. Of the glomeruli, a certain number 
remain of normal size, but with the tuft-cells swollen or 
multiplied. Many others are found in all stages of atrophy 
until they are converted into little fibrous balls. The atro¬ 
phy seems to depend partly on the growth of tuft-cells and 
intercapillary cells, partly on the thickening of the capsules, 
partly on the occlusion of the arteries. If the chronic 


CHRONIC BRIGHT'S DISEASE. 


641 


nephritis follows chronic congestion, the glomeruli remain 
large, but with a marked growth of tuft-cells; or they be¬ 
come atrophied, but with the dilatation of the capillaries 
still evident. The capillaries of the glomeruli may be the 
seat of a waxy degeneration. The arteries exhibit the same 
changes as are found in chronic exudative nephritis.” 

Complicating- Lesions.—Hypertrophy of the left ventri¬ 
cle of the heart is almost constant, and affords corroborative 
aid in diagnosis. The hypertrophy may be followed by 
dilatation, chronic degeneration, or myocarditis. 

General arterio-sclerosis is frequently found associated 
with the nephritis. Chronic endocarditis may complicate 
the disease. In some cases the heart-lesion is primary, 
being followed by chronic congestion of the kidney and by 
nephritis. In other cases the cardiac and renal changes 
occur together in the same patient and are due to the same 
causes, but are not directly dependent on each other. 

Endarteritis with hypertrophy of the heart may give rise 
to cerebral hemorrhage. 

Emphysema and cirrhosis of the liver may be found asso¬ 
ciated with the nephritis, all being types of chronic produc¬ 
tive inflammation due to the same causes. 

Pericarditis is not uncommon, and should be suspected 
in all nephritis cases dangerously sick with obscure symp¬ 
toms. There seems to be an increased liability to gastritis 
and bronchitis. 

Symptoms.— 1. Urinary .—The urine is usually increased 
in quantity, is of a light-yellow color, has a specific gravity 
ranging between 1005 and 1010, and contains a diminished 
amount of urea to the ounce. Albumin and casts are usu- 
aily absent, or albumin is present only in traces, especially 
in the early morning urine. During the acute exacerbations 
of the nephritis, or in the latter stages when the heart be¬ 
gins to fail, albumin and casts may be present in consider- 

41 


642 MANUAL OF THE PRACTICE OF MEDICINE. 

able quantities. In exceptional cases the specific gravity 
may be normal, or it may be exceedingly low, ranging be¬ 
tween 1001 and 1003, with or without waxy degeneration 
of the vessels. During the acute exacerbations of the 
nephritis and during the attacks of contraction of the arteries 
the urine may be scanty or even suppressed. In rare cases 
there may be blood in the urine, or even profuse bleeding 
from the kidneys. 

2. Cerebral symptoms appear in the majority of the cases, 
and are due to a variety of causes : 

(a) Headache, usually frontal, and sleeplessness are com¬ 
mon ; the headache may be so severe that the patient is 
almost beside himself. There may be in various parts of 
the body neuralgic pains difficult of relief. Muscular twitch- 
ings and general convulsions are of serious import. There 
may be delirium, mild or furious, or stupor and coma. 
When these cerebral symptoms come in attacks the arteries 
are contracted, the heart’s action is labored, and the temper¬ 
ature is raised. To this condition the name “ acute uraemia ” 
is given. From such an attack the patient may die, or he 
may recover, but the attack is liable to be repeated. These 
attacks may occur early or late in the disease, and such an 
attack may even be the first symptom noticed. 

(b) Delirium and stupor may come on gradually in the 
latter part of the disease, with a feeble, low-tension pulse 
and a tendency to a subnormal temperature. These symp¬ 
toms are due to chronic uraemia. 

( c ) There may be the symptoms of cerebral hemorrhage, 
coma, hemiplegia, and possibly of aphasia. 

( d ) There may be attacks of hemiplegia or aphasia, with 
coma which may persist until death or disappear in a few 
days. These symptoms appear to be due to endarteritis of the 
cerebral vessels, and not to any changes in the brain-tissue. 

3. Circulatory Symptoms .—The pulse is hard and of an 


CHRONIC BRIGHT'S DISEASE. 643 

increased tension. Thickening of the arterial wall from 
endarteritis may render the artery less compressible, and 
should not be mistaken for an actual increase in tension. 
A low-tension pulse is not a favorable symptom. The left 
ventricle is almost invariably found hypertrophied, and the 
second aortic sound is accentuated. Should dilatation or 
heart-weakness occur, the pulse will fall in tension and 
signs of venous congestions will appear, so that the con¬ 
dition will resemble that of a chronic heart-lesion. A great 
deal can be done by appropriate treatment to prevent dila¬ 
tation from occurring. 

4. Respiratory Symptoms .—Dyspnoea is frequently the 
first symptom noticed, appearing in spasmodic attacks 
aggravated by exertion or by the recumbent position. The 
attacks may last for minutes, hours, or days. The spas¬ 
modic dyspnoea appears to be due to an association of con¬ 
tracted arteries with a feeble or dilated heart. Dyspnoea 
more or less steady may also be due to chronic uraemia, 
anaemia, pleural effusion, or pericarditis. There may be 
Cheyne-Stokes breathing toward the close of the disease— 
a most unfavorable symptom. Bronchitis, especially dur¬ 
ing the winter, is exceedingly common; pleurisy and pneu¬ 
monia are not uncommon. There may be sudden oedema 
of the glottis or of the lung, especially during acute uraemic 
attacks. Emphysema frequently coexists and adds its symp¬ 
toms to the clinical history. 

5. Gastro-intestinal Symptoms .—There maybe attacks of 
catarrhal gastritis or of spasmodic vomiting, which may be 
severe and uncontrollable, endangering the life of the patient. 
Loss of appetite and dyspeptic symptoms are common. 
There may be severe diarrhoea, which to a certain extent 
appears to be compensatory, aiding in the elimination of the 
urea, and therefore it should not be checked too rapidly 
unless it be excessive and exhausting. 


644 MANUAL OF THE PRACTICE OF MEDICINE. 

6. Special Senses .—Sudden blindness—“ uraemic amauro¬ 
sis ”—may occur without retinal changes, and may be 
temporary or permanent. Neuro-retinitis or retinitis albu- 
minurica, with white specks and flame-shaped hemorrhages, 
with or without thickening of the retinal vessels, may occur 
as the initial symptom, and many cases of nephritis are 
often first diagnosed by the ophthalmologist, to whom the 
patient applies for relief from the troubles in vision. Ring¬ 
ing in the ears with dizziness is not uncommon, and deaf¬ 
ness may occur. 

7. Skin .—There may be some puffiness of the ankles 
from time to time, but this symptom is not common, and 
dropsy does not occur unless it be the result of a failing 
heart. The skin is usually dry, and sweating is not com¬ 
mon. In bad cases of uraemia urea may be excreted, giving 
a frosted appearance to the skin. There may be purpura in 
cachectic conditions. 

8. General Condition .—The blood becomes anaemic, but 
this is not as marked as in the cases with exudation. The 
nutrition is affected, so that there is a gradual loss of flesh 
and of strength. 

Course of the Disease. —At autopsy from some intercur¬ 
rent disease the lesion may be found in a fairly advanced 
form without having given appreciable symptoms during 
the life of the patient. 

2. Some patients go for years with a urine of low specific 
gravity, with a hypertrophied left ventricle, with accentuated 
second aortic sound, and with habitual increase of arterial 
tension, and yet feel perfectly well. Upon these symptoms, 
however, a diagnosis can with certainty be made. Any 
persistent high tension of the pulse with thickening of the 
arterial wall in a patient under fifty years of age points to 
cardio-vascular, and probably to renal, changes. 

3. There may be, from time to time, attacks of acute 


CHRONIC BRIGHT'S DISEASE. 645 

uraemia, with contracted arteries, increased blood-tension, 
and cerebral symptoms. The urine is scanty and contains 
albumin. Each succeeding attack is apt to be more severe, 
and between the attacks the general health depreciates and 
the patient becomes feeble and emaciated. 

4. There may be no symptoms for a long time, the first 
evidence of disease being an attack of acute uraemia from 
which the patient may or may not recover, or of cerebral 
endarteritis or cerebral hemorrhage. 

5. In some cases a gradual loss of flesh and of strength 
with digestive disturbances and low specific gravity of the 
urine may be the only symptoms until the time of the 
patient’s death. The only symptom pointing to the kidney 
is the low specific gravity of the urine. 

6. The kidney-lesion may give no direct symptoms; but 
should the hypertrophied heart begin to dilate and nervous 
congestion appear, the picture will be that of the last stages 
of heart disease, and the primary kidney-lesion will be over¬ 
looked. Many of the so-called cases of “ idiopathic dilata¬ 
tion ” arise in this way. 

Prognosis. —The disease is absolutely incurable, but it is 
not incompatible with the enjoyment of a busy life for a 
number of years. Cases have been followed for ten or 
fifteen years. Much depends upon how much care the 
patient will take of himself, and how carefully dilatation 
and heart-failure are guarded against. 

Treatment. —General Treatment .-—Much good can be 
done by regulating the diet and the mode of life and by 
selecting a suitable climate. The diet should be light and 
nourishing, but not excessive. Meat should be taken but 
once a day, but the ingestion of fats should be encouraged. 
Alcohol should be prohibited; tea and coffee may be 
allowed in moderation. The urinary secretion should be 
kept free by drinking a certain amount of distilled water or 


646 MANUAL OF THE PRACTICE OF MEDICINE. 


some mineral water like Poland. The bowels should be 
kept freely open ; the skin is to be kept active by daily baths 
and friction; and exercise in the open air should be encour¬ 
aged in proportion to the strength. Much is gained by 
spending the winter months in some warm, equable climate. 
Severe mental or physical work should be avoided, so as to 
lessen the strain on the heart and the arteries. Anaemia is 
to be treated by iron. 

Heart and Arteries .—A certain increase in tension is 
allowable. Excessive tension should be reduced by an 
occasional saline laxative and hot bath. Of the arterial 
dilators, the best are nitroglycerin (gr. three times a 
day, increased, if necessary, until the desired effect is pro¬ 
duced), potassium iodide (gr. x three times a day), and 
chloral hydrate (gr. v-viij three times a day). Not only is 
the tension thus reduced, but headache, dizziness, and dysp¬ 
noea are often relieved in a most satisfactory manner. For 
restlessness morphia in small doses at night may be used. 
Should the heart’s power fail and the tension be low, stimu¬ 
lants are needed as in cardiac disease—caffeine, digitalis, 
strychnine, and strophanthus. Opium is contraindicated 
in these cases, as small doses frequently cause fatal poi¬ 
soning. 

Ureemia .—Acute uraemia being due to contracted arteries, 
arterial dilators are indicated in free doses. The bowels 
should be opened rapidly, and in case of convulsion or 
coma bloodletting is frequently followed by brilliant results. 
Hypodermic injections of from •J- to \ grain of morphia may 
be used in convulsions or coma with benefit, and for the 
convulsions whiffs of chloroform may be needed. 

Chronic uraemia being due to retention of excrementitious 
substances, effort should be made to increase their elimina¬ 
tion. The kidneys should be stimulated by digitalis com¬ 
bined with the saline diuretics; cups and poultices over the 



WAXY DEGENERATION OF THE KIDNEY. 647 


kidneys should be employed in bad cases. The bowels 
should be opened energetically, and sweating is to be in¬ 
duced by the hot pack or the hot-air bath. 

Acute exacerbations should be treated on the lines laid 
down for acute nephritis. 


WAXY DEGENERATION OF THE KIDNEY 
(AMYLOID KIDNEY). 

Waxy degeneration of the kidney does not appear as a 
disease by itself, but as an added degeneration to the lesions 
of chronic diffuse nephritis, usually of the form with exuda¬ 
tion. It occurs in cases with prolonged suppuration, espe¬ 
cially of the bones, with syphilis and tuberculosis, occa¬ 
sionally with leukaemia, and in rare cases without apparent 
cause. It is associated with amyloid degeneration of the 
spleen and the liver. 

Pathology.—There are usually the appearances of the 
“ large white,” more rarely of the “ small white,” kidney. 
The glomeruli are distinct and have a bacon-like lustre, 
staining mahogany-brown with weak, watery solutions of 
iodine, and red with dilute solutions of methyl-violet. The 
amyloid degeneration involves the vessels of the glomeruli, 
of the vasa recta, and occasionally of the membrane of the 
uriniferous tubules. 

Symptoms. —The urine is usually abundant, pale, and of 
a low specific gravity. Albumin is usually present in con¬ 
siderable quantity, and there may be globulin. Tube-casts 
frequently include hyaline varieties which give the amyloid 
reaction. The general symptoms are those of the associated 
nephritis, together with the original suppurative or cachectic 
disease to which the amyloid changes are secondary. The 
diagnosis is aided by the detection of waxy changes in the 
liver and the spleen. 


648 MANUAL OF THE PRACTICE OF MEDICINE. 


TUBERCULAR DISEASES OF THE KIDNEY. 

Tuberculosis of the Kidney. 

Miliary tubercles are frequently found in the kidney in 
cases of general miliary tuberculosis. The tubercles are 
small, are unaccompanied by inflammatory changes, and 
do not give rise to symptoms. 

Tubercular Pyelonephritis. 

Etiology. —The tubercle bacilli may infect the kidney 
through either the blood-vessels or the urinary passages. 
The infection may in rare instances be primary, but the 
ordinary cases are secondary to a tubercular focus else¬ 
where, especially in the bladder, the prostate, or the seminal 
vesicles. In many cases it is impossible to say whether a 
primary tuberculosis of the kidney has been followed by 
secondary tubercular lesions in the genito-urinary tract, or 
whether the kidney-lesions have followed infection creeping 
up the ureters from a primary focus below. 

Tubercular disease of the kidney is twice as frequent 
in men as in women, and it is most frequent in those of 
middle age. 

Pathology. —The lesion usually begins in the pelvis of 
the kidney. The pelvis becomes dilated and is filled with 
pus and cheesy material ; its walls are thickened, infiltrated 
by pus and tubercle-tissue, and its mucosa becomes increased 
in thickness. Tubercular infiltration extends to the kidney- 
tissue and rapidly undergoes cheesy degeneration and soften¬ 
ing, so that the kidney becomes honeycombed with cavities. 
In advanced cases the kidney is converted to a cyst contain¬ 
ing inspissated cheesy matter infiltrated with lime-salts. Both 
kidneys are usually involved, but the disease is usually 
more advanced on one side than on the other. In other 
cases one kidney alone is involved, the kidney of the oppo- 


TUBERCULAR DISEASES OF THE KIDNEY. 649 


site side developing the lesions of chronic diffuse nephritis 
with exudation usually with waxy changes. 

In the majority of cases tubercular disease of the kidney 
is complicated by similar tubercular changes in the ureter 
and the bladder, and sometimes in the prostate gland and 
the seminal vesicles as well. 

Symptoms. — 1. Urinary symptoms consist in the fre¬ 
quent appearance in the urine of pus, cheesy material, fatty 
epithelial cells, and shreds of kidney-tissue. There may 
be occasional admixture of blood. These urinary changes 
also occur with calculous pyelo-nephritis, and so possess no 
absolutely diagnostic value. The discovery of tubercle 
bacilli, however, in the urine is an infallible sign of tuber¬ 
culosis. The bacilli are best found in the small particles 
of cheesy matter present in the sediment. Albuminuria is 
usually more marked than can be accounted for by the pus. 
Tube-casts are of rare occurrence. 

2. Local symptoms consist of pain and tenderness over the 
affected kidney. The pain may be dull and continuous or 
it may be paroxysmal, resembling renal colic; in the latter 
case it is due to the passage of lumps of cheesy material 
along the ureter. 

3. An enlargement of the kidney may be appreciated in 
some instances, as in calculous or suppurative pyonephritis, 
but as the enlargement is rarely decided, it is with diffi¬ 
culty detected. 

4. The constitutional symptoms are those of other tuber¬ 
cular diseases. Fever is rarely absent, and usually presents 
a remitting hectic character. Anaemia, emaciation, and 
weakness increase with the progress of the disease. 

5. There may be complicating tubercular diseases else¬ 
where which add their characteristic symptoms. Acute 
miliary tuberculosis not infrequently develops. 

Diagnosis. —The diagnosis from calculous pyelonephritis 


650 MANUAL OF THE PRACTICE OF MEDICINE. 

is made (1) by the presence of tubercular disease elsewhere, 
especially in the lower genito-urinary organs ; (2) by the 
absence of a history of renal calculi; (3) by the presence 
of the tubercle bacilli in the urine. 

Prognosis. —The course of the disease is progressive. 
The great majority of cases terminate fatally within two 
years, but it is possible for the disease to stop and the 
patient to recover. 

Treatment. —Surgical treatment consists in the removal 
of the diseased kidney, and this should be done before other 
portions of the genito-urinary tract become infected ; hence 
an early diagnosis is of the greatest importance, and it 
should be a rule to examine for tubercle bacilli in every 
case of persistent pyuria, so that incipient cases of tubercular 
kidney may thus be recognized. 

SUPPURATIVE DISEASE OF THE KIDNEY 
(SURGICAL KIDNEY). 

Etiology. —The germs of suppuration may gain access 
to the kidney—(1) through the abdominal wall, as with 
penetrating wounds; (2) by extension from neighboring 
abscesses; (3) through the blood-vessels, as in pyaemia and 
malignant endocarditis; and (4) through the ureter, as from 
cystitis or following operations upon the genito-urinary 
organs. The first two methods of infection are exceedingly 
rare. Infection through the ureter is favored by inflam¬ 
matory conditions of the urinary passages, by pyelitis, 
whether simple, tubercular, or calculous, and by injuries 
and contusions of the kidney. 

Suppuration of the kidney alone is termed “ suppurative 
nephi itis, but as the pelvis of the kidney is almost regularly 
involved, the name “ pyelo-nephritis ” is often applied. 
Should the pelvis of the kidney be distended with pus, the 
term “pyonephrosis” is not inappropriately applied. 


SUPPURATIVE DISEASE OE THE KIDNEY. 65 I 

The cases of suppurative pyelo-nephritis complicating 
tubercular disease and calculi in the pelvis of the kidney 
will be considered when discussing these diseases. 

Pathology and Symptoms.— 1. Abscisses produced by 
emboli may occur in the course of pyaemia and malignant 
endocarditis. Both kidneys are large, congested, and 
studded with small abscesses. The blocking of small ter¬ 
minal arteries by the emboli causes pyramidal areas of white 
infarctions which subsequently break down to form abscesses. 

The symptoms of embolic abscesses in the kidney are 

obscured by those of the primary disease. Pus may not 

appear in the urine, as the abscesses seldom communicate 

with the urinarv tubules. 

* 

2. Idiopathic abscesses occur without assignable cause, 
and it is unknown whether the suppuration begins first in 
the kidney or in its pelvis. One kidney becomes partially 
destroyed, and in the remaining portion abscesses are found. 
The pelvis of the kidney is inflamed and becomes dis¬ 
tended with pus, constituting a pyonephrosis. The sup¬ 
purative processes may extend to the perinephritic tissues. 

The symptoms are at first obscure: 

(a) Pus-symptoms are present, consisting of irregular 
fever, erratic chills, and cold sweatings. The symptoms of 
septicaemia or of the typhoid condition may become marked, 
or the patient will develop the waxy changes in the viscera 
that regularly accompany prolonged suppuration. 

(b) Symptoms of a localized abscess consist of pain and 
tenderness over the kidney. 

(c) Pus and broken-down kidney-tissue are present in the 
urine. The urine is frequently acid, the pus is uniformly 
mixed with the urine, and the character of the urine is 
unchanged after the bladder has been washed out. From 
time to time the pus escapes from the dilated pelvis in large 
quantities and appears in the urine. 


652 MANUAL OF THE PRACTICE OF MEDICINE. 


( d ) There may be a tumor, appreciable by palpation 
should the pelvis of the kidney be sufficiently distended 
by pus. The tumor may become reduced in size by the 
escape of pus in large quantities down the ureters. 

3. Suppurative Pyelonephritis from Cystitis .—Both kidneys 
are swollen, congested, and studded with small foci of in¬ 
flammation. The pelvis of the kidney is inflamed and 
coated with fibrin and pus. By the confluence of the sup¬ 
purative foci large portions of the kidneys are converted to 
abscesses. The ureters may be normal or they may be 
inflamed. The lesions of an acute or chronic cystitis are 
almost always present. 

In some cases there is an antecedent history of cystitis. 
At the time of the kidney-infection, the patient will develop 
septic symptoms—repeated chills and irregular fever with 
prostration. The urine will be diminished and will contain 
pus and blood from the bladder or kidney or from both. In 
some cases the urine is altogether suppressed. Prostration 
becomes more extreme, and the patient dies with pyaemic 
or septic symptoms. 

4. According to Delafield, suppurative nephritis following 
cystitis due to enlarged prostate presents a different clini¬ 
cal picture. The patients are men, usually over fifty years 
of age, who have suffered from cystitis and an enlarged 
prostate gland. The first symptom is a diminished quan¬ 
tity of urine containing blood, or blood alone may seem to 
be passed. In other cases the urine is altogether suppressed. 
The patient becomes restless, anxious, and shows an increas¬ 
ing prostration; there are usually no chills, and there may 
be no fever. The patient may either die in collapse within 
a few days or may die from septic poisoning. 

The prognosis is always fatal if both kidneys be involved. 
If one kidney alone be the seat of abscess, it may be removed 
and the patient may recover. 


TUMORS OF THE KIDNEY. 


653 


Treatment.—The preventive treatment is directed toward 
the cystitis and toward strict asepsis in all operations upon 
the urinary organs. When symptoms of suppurative 
nephritis occur, it is of the greatest importance to decide 
whether one or both kidneys be involved. The position 
of localized tenderness is to be considered, but the surest 
method of settling the question is by cystoscopic examina¬ 
tion. If by the cystoscope purulent urine be seen to flow 
from both ureters, operative treatment is of no avail. If the 
pus be seen to flow from one ureter alone, the prospects of 
recovery after the operation are rendered more probable. 

TUMORS OP THE KIDNEY. 

Benign tumors consist of fibroma, lipoma, lymphade- 
noma, and adenoma. These benign growths are of little 
clinical interest. 

Malignant tumors are sarcoma and carcinoma. 

Sarcoma may occur in adult life, but it is more frequent 
in young children, and not infrequently it occurs as a con¬ 
genital tumor. The ordinary form of sarcoma is the small- 
celled variety ; a rarer form, usually of congenital origin, is 
the rhabdo-myoma, which consists of sarcoma and striped 
muscular fibre. Sarcoma of the kidney grows rapidly, is 
very vascular, and frequently breaks down in places to form 
cysts containing blood and clots. 

Carcinoma is usually of the encephaloid variety, and so 
frequently shows an alveolar structure that it has been 
described as “ malignant adenoma.” 

Secondary cancer of the kidney is not uncommon, with 
a primary growth situated in the testicle or the prostate 
gland. In the secondary form both kidneys are usually 
studded with small isolated nodules. 

Primary malignant growths of the kidney frequently reach 
enormous dimensions, so as to cause symptoms by pressure 


654 MANUAL OF THE PRACTICE OF MEDICINE. 

upon the abdominal organs. Pressure on the ureter fre¬ 
quently results in a hydronephrosis. Secondary deposits 

may occur by extension 
or metastasis. 

Symptoms consist of 
pain and tenderness, hae- 
maturia, cancerous ca¬ 
chexia, and the presence 
of an abdominal tumor. 

Pain and tenderness are 
not constantly present. 
The pain may be steady 
and dull, radiating to the 
groin and the thigh, or 
there may be a parox¬ 
ysmal pain, due to the 
passage of a blood-clot 
down the ureter, resem¬ 
bling the pain of renal 
colic. 

Hcematuria occurs in 
about half the cases, and 
may be the first symp¬ 
tom noticed. The blood, 
when present, is usually constant. There may be blood- 
casts of the pelvis of the kidney and of the ureter \ these 
casts are very characteristic of cancer. The blood is usually 
passed in small quantities, although exhausting or even fatal 
hemorrhages may occur. 

The symptoms of malignant cachexia become progres¬ 
sively marked. Anaemia is rendered more profound by the 
occurrence of hemorrhage; emaciation is extreme, and is in 
marked contrast to the enlarged abdomen. 

o 

The tumor is at first located in the region of the kidney, 



Fig. 49. —Sarcoma of kidney. Perfect health 
after operation (Abbe). 











CYSTS OF THE KIDNEY. 


655 

but it tends later to invade the whole abdominal cavity. It 
may be distinguished by the following peculiarities : (a) The 
surface often presents a series of convexities or knobs ; (li) 
there is no respiratory movement of the growth, and (e) the 
hand may usually be thrust between it and the free border 
of the ribs; (d) the growth is not movable, as is a floating 
kidney; (e) percussion shows the colon passing in front of 
the growth ; (/) a tympanitic zone is usually detected by 
percussion between the liver and the neoplasm; (g) rapid¬ 
growing tumors may yield a sense of fluctuation; (li) the 
renal tumor can usually be traced deeply into the loin. 

In children the diagnosis of the growth from retroperito¬ 
neal sarcoma may be impossible. 

The duration of malignant growths of the kidney is vari¬ 
able. The congenital cases may terminate fatally within a 
few weeks after birth. Usually in children the course is 
more rapid and malignant than in adults, seldom extending 
over one year. More rarely the disease may exist for a 
number of years before death occurs. 

The prognosis is uniformly bad unless an early and 
successful nephrectomy be performed. 

Treatment.—The results of nephrectomy for sarcoma in 
children are not good. The operation, however, should be 
performed if the diagnosis be made early in the disease, and 
in cases in which the disease is limited to the kidney. In 
adults the results of the operation are somewhat more en¬ 
couraging. The risks of the operation itself are great, 
shock and hemorrhage being the imminent dangers en¬ 
countered. 


CYSTS OF THE KIDNEY. 

Etiology and Pathology. — Small retention-cysts of the 
kidney are common in chronic nephritis; they may also 
occur in comparatively healthy kidneys. 


656 MANUAL OF THE PRACTICE OF MEDICINE. 


Congenital Cystic Kidney .—The kidneys are enlarged 
and are converted into a mass of cysts of all sizes, separated 
by septa of connective tissue or of compressed kidney- 
structure. The cysts contain a clear fluid holding the 
urinary salts in solution, or the fluid may be brownish and 
turbid. Albumin, blood, uric-acid crystals, and cholesterin 
are often found in these cysts. Congenital cystic kidney is 
probably the result of defective development, but how the 
cysts actually originate is not known. 

In adults multiple cysts may be found in the kidneys. 
The cysts contain clear or brownish serum or colored 
matter. Similar cysts are sometimes found in the liver and 
the spleen. The origin of these cysts is unknown, although 
it has been surmised that they are congenital. 

Symptoms. —Cysts of the kidney give of themselves no 
characteristic symptoms except in rare cases of rupture. 
Symptoms of chronic diffuse nephritis are usually present, 
and death may finally result from uraemia. 

Treatment is useless. 


PYELITIS. 

Etiology. —Inflammations of the pelvis associated with 
suppuration of the kidney, renal calculi, and tubercular 
disease have elsewhere been described. 

Besides these forms, pyelitis may develop after the use of 
turpentine, cubebs, and cantharides, and from the irritation 
of saccharine or decomposing urine within the pelvis. 
Secondary pyelitis may complicate typhoid fever, diphtheria, 
and the exanthemata. Chronic catarrhal pyelitis may result 
from cystitis, from hydronephrosis, or from the continuance 
of an acute attack. In some cases the cystitis may develop 
without apparent cause. 

Pathology. —The mucous membrane of the pelvis is 
thickened, infiltrated, and coated with mucus or with muco- 


H YDR ONEPHR OS IS. 


65 7 

pus. Phosphatic calculi may form as the result of the in¬ 
flammation. In some cases the inflammation spreads to the 
kidney, so that a pyelo-nephritis results. 

Symptoms. Pain and tenderness are referred to the 
kidney. The urine is generally acid in reaction and con¬ 
tains pus, mucus, epithelial cells from the pelvis of the 
kidney, and occasionally blood. The pyuria may be con¬ 
stant or intermittent. If suppuration extend to the kidney 
itself, the symptoms of suppurative pyelo-nephritis or of 
pyonephrosis will be developed. 

The diagnosis from tubercular pyelo-nephritis is made 
by the absence of tubercular foci in other parts of the body 
and by the absence of tubercle bacilli in the urine. The 
course of the tubercular form of pyelitis is more serious, 
and the disease usually terminates fatally. The diagnosis 
from calculous pyelitis cannot be made in all cases, but a 
long history of renal calculi affords an important clue to the 
diagnosis, and pyelitis is to be considered calculous if 
crystals of uric acid or of oxalate of lime be more or less 
continuously present in the urine. 

Treatment consists in giving bland alkaline mineral 
waters or citrate of potassium in doses sufficient to render 
the urine neutral in reaction. The diet should be unirritat- 
ing, and drugs that are capable of causing irritation or con¬ 
gestion of the kidney should not be given. If suppurative 
pyelo-nephritis occur, surgical treatment is indicated. 

HYDRONEPHROSIS. 

Etiology.—When any obstruction arises in the urinary 
tract, interfering with the free passage of urine, the pent-up 
urine causes an increasing dilatation of the urinary parts 
above the contraction. A contraction of the ureter may 
result from impacted renal calculi, from bends, from cica¬ 
tricial contraction, or from external pressure, especially by 
42 


658 MANUAL OF THE PRACTICE OF MEDICINE. 
new growths of the uterus or the ovaries. The lower 

o 

orifice of the ureter may be stenosed in cancer of the 
bladder. In some cases congenital hydronephrosis results 
from congenital membranous obstruction or from abnormal 
valve-formations of the ureter. Double hydronephrosis, 
which results from strictures of the urethra, may also occur 
with enlargement of the prostate gland, or even with 
phimosis. Double hydronephrosis is regularly accom¬ 
panied by dilatation of the bladder and of both uieters. 
The more gradually the obstruction is developed, the 
greater the degree of the dilatation ; and it is impoitant 
to remember that a sudden complete obstruction of a 
ureter, as by a renal calculus, does not lead to hydrone¬ 
phrosis, but to atrophy of the kidney. 

Pathology. —The pelvis of the kidney is dilated; pres¬ 
sure-atrophy of the kidney-tissue results, and in the com¬ 
pressed kidney a chronic nephritis is set up. In advanced 
cases the kidney becomes converted to a cyst, in whose 
wall may be seen a thin rind of atrophied and com¬ 
pressed kidney-tissue. The fluid is thin and yellowish, and 
contains urea, uric acid, and sometimes albumin. It may 
be turbid from the admixture of pus. In cases of long 
duration the urinary salts may disappear, so that the fluid 
may not be characteristic. In extreme cases the sac may 
contain from ten to twenty quarts of fluid. 

Symptoms. —The majority of cases give rise to no symp¬ 
toms except the presence of a tumor, which first appears in 
the region of the kidney and enlarges toward the hypo- 
chondrium and the median line. Fluctuation may be 
appreciated in some cases. The colon lies in front of the 
cyst, and may be recognized by the tympanitic percussion- 
note obtained over it. The size of the tumor varies from 
time to time according to the amount of urine passed. In 
the rare cases of “ intermittent ” hydronephrosis the tumor 


NEPHR OL1THIA SIS. 


659 


may entirely disappear, with the discharge of its contents 
down the ureter. These cases, which are frequently con¬ 
genital, appear to be due to a valve-like orifice of the ureter, 
which is opened only when the walls of the pelvis of the 
kidney are dilated and put upon the stretch. In other 
intermitting cases the ureter arises from the upper portion 
of the pelvis. Aspiration of the tumor differentiates 
hydronephrosis from solid growths, and the character of 
the aspirated fluid may confirm the diagnosis. In other 
cases intermittent hydronephrosis occurs with movable 
kidney. The growth of the tumor may give rise to pres¬ 
sure-symptoms, nausea and vomiting, and to shooting pains 
extending down the thigh. Uraemic symptoms may occur 
with bilateral hydronephrosis and in cases in which nephritis 
occurs in the dilated kidney. Suppuration may result in 
the formation of a pyonephrosis. 

Prognosis. —Death may result from the primary disease, 
from secondary hydronephrosis, or from uraemia. Recovery 
may follow if the cause of the obstruction be removed; it 
may also follow operative interference. 

Treatment is surgical. When the sac reaches large size 
the fluid may be removed by aspiration, or the sac opened 
and drained. The kidney may be extirpated as a last resort. 

NEPHROLITHIASIS; RENAL CALCULI. 

Etiology. —The solid constituents of the urine may be 
deposited in the kidney itself in several forms, to which the 
name “infarcts” has been incorrectly applied. 

1. Uric-acid infarcts occur as reddish streaks at the bases 
of the pyramids in new-born children aftei the fourteenth 
day. They are not found in stillborn children. 

2. Infarcts of sodium urate, with occasionally ammonium 
urate, appear as whitish lines at the apices of the pyramids 
in gouty kidneys. 


660 MANUAL OF THE PRACTICE OF MEDICINE . 


3. Lime infarcts, seen in the kidneys of old people, 
appear as white lines in the pyramids. 

The term “ calculi ” should more properly be confined to 
the concretions formed within the pelvis of the kidney. 
These calculi are common to all ages and are more frequent 
in males than in females. The occurrence of calculi of uric 
acid or of oxalate of lime is favored by gouty conditions 
and by functional disturbance of the liver. Phosphatic 
calculi are more commonly associated with inflammations 
of the pelvis of the kidney. Diet seems to exert no direct 
influence upon the formation of renal concretions, but the use 
of hard drinking-water containing lime seems to predispose 
to their formation. The deposition of uric acid, according to 
Roberts, is favored by the following urinary conditions: (1) 
High acidity; (2) poverty of salines; (3) low pigmentation; 
(4) high percentage of uric acid. 

Pathology.—The important varieties of calculi are as 
follows: (1) Uric acid alone or combined with concentric 
layers of the urates; (2) uric acid with alternating layers of 
lime oxalate ; (3) lime oxalate alone (“ mulberry calculus ”); 
(4) phosphatic calculi of the magnesium salts, of the ammonio- 
magnesium salts, or of both ; (5) urates alone, especially in 
children; (6) cystin, resulting in a soft concretion of bees¬ 
wax consistency. A central nucleus is occasionally found, 
consisting of mucus or of a small blood-clot. 

The ordinary size of the calculi varies from small gritty 
particles—“ renal sand ”—up to the size of rice-grains. In 
the pelvis of the kidney there may be found larger calculi 
of an irregular branching shape—the so-called “ dendritic 
calculi.” Calculi forming perfect stony casts of the renal 
pelvis have been described. Uric-acid and oxalate-of-lime 
calculi are more apt to be formed in both kidneys than are 
those of phosphatic origin. 

Symptoms are produced by (1) the passage of the cal- 


NEPHR OL1THIA SIS. 661 

cuius down the ureter; (2) its retention in the ureter; (3) 
its retention in the pelvis of the kidney. 

1. Passage of the Calculus through the Ureter. —Small 
concretions may pass without symptoms, or may give rise 
to twinges of pain in the side, the pain running down to the 
bladder. Larger calculi, entering the ureter, are pushed 
downward in jerks by the pressure of urine behind them, 
and give rise to the symptoms of renal colic. 

Symptoms of Renal Colic. — (a) Pain is severe, steady, 
located in the side or the back, with cutting or tearing ex¬ 
acerbations which radiate downward to the groin and tes¬ 
ticle. Radiation upward does not occur. The testicle may 
be swollen and retracted. The pain appears suddenly, and 
disappears with equal abruptness when the calculus drops 
into the bladder. The pain is often so intense that the pulse 
becomes rapid, feeble, and irregular. Syncope and vomiting 
are commonly observed. Convulsions may occur in chil¬ 
dren. In some cases there are chilly feelings with a mod¬ 
erate fever during the attack. 

($) Urinary Symptoms. —There is a constant desire to 
micturate, and the act may be painful from an associated 
spasm of the neck of the bladder. The urine, which is 
usually scanty, may contain blood. It may be suppressed 
either from functional inhibition or from previous calculous 
disease with atrophy of the opposite kidney. In some cases 
the urine is copious and limpid. After the attack dull, 
aching pain, with some tenderness over the kidney, continues 
for several days. 

2. Impaction of the Calculus within the Ureter. —The attack 
begins as renal colic; the cutting paroxysms of pain grad- 
uallv cease, and the dull ache alone remains for a consider- 

able time, and finally disappears. 

(a) The calculus may finally be passed after a period of 
impaction. This fortunate occurrence is more common if 


662 MANUAL OF THE PRACTICE OF MEDICINE. 

several calculi are impacted within the ureter. The passage 
of the obstruction is accompanied by the symptoms of renal 
colic, usually with blood in the urine, and may be followed 
by the passage of an excessive quantity of urine, especially 
if the other kidney have previously been disabled by calcu¬ 
lous disease. In one case of the writer’s, in which atrophy 
of the left kidney had taken place by a previous impaction 
of a calculus in its ureter, impaction in the right ureter oc¬ 
curred, with anuria of twelve days’ duration. The final 
passage of two small calculi was followed by the excretion 
of eighteen pints of urine containing over five ounces of 
urea, the diuresis not being due to the drainage of a hydro¬ 
nephrosis. 

{ 6 ) If the calculus remain, completely obstructing the 
duct, urinary secretion of the kidney will cease as soon as 
the pressure of the pent-up urine equals the blood-pressure 
within the renal artery. The kidney undergoes atrophy, 
and is converted to a little cyst in whose walls may be seen 
a thin shell of kidney-tissue. The cyst contains from one- 
fourth to one-half an ounce of clear serum, or the contents 
may consist of inspissated pus containing calculi and lime- 
salts. The ureter above the impaction becomes converted 
to a fibrous cord. Hydronephrosis never occurs if the ob¬ 
struction be sudden and complete. 

The symptoms of such an atrophy of the kidney depend 
entirely upon the condition of its companion organ. If the 
remaining kidney be in good condition, it will be able to 
do the extra amount of work required of it, and no symp¬ 
toms will be developed. If the other kidney, however, be 
destroyed in like manner by previous calculous disease, or, 
as has happened, if there be but one kidney, then anuria 
develops. The characteristic of this obstructive anuria is 
that it may exist for a number of days without marked 
uraemic symptoms. Finally, at the end of one or two weeks 


NEPHROLITHIASIS. 66 3 

uraemic symptoms develop, or the patient may suddenly 
die. 

In some cases pressure-necrosis of the ureter at the point 
of impaction allows of perforation and of peritoneal sepsis. 

If the impaction be incomplete, so that gradual back¬ 
pressure is exerted upon the pelvis of the kidney, hydro¬ 
nephrosis may be developed. I his, however, is a slow and 
gradual process. 

3. If the calculi remain in the pelvis of the kidney , they 
tend to grow larger and to assume the form of the cavity 
in which they lie. There results from their presence either 
a pyelitis, mild, severe, or suppurative, or dilatation of the 
pelvis (pyonephrosis), or a suppuration of the kidney (pyelo¬ 
nephritis). 

Mild forms of pyelitis result in pain , of a dull, aching 
character, usually increased by exertion. The pain is 
usually referred to the kidney or to the back, but it may be 
referred to the opposite kidney—a point which should be 
remembered in operating upon such cases. From time to 
time there occur attacks of renal colic with its characteristic 

pain. 

Tenderness over the kidney is usually detected by bi¬ 
manual palpation. 

The urine, which is generally acid in reaction, contains 
mucus, epithelial cells from the pelvis of the kidney, blood, 
pus-cells, and crystals of uric acid or of oxalate of lime. 
Hoematuna is not profuse, but is apt to be persistent, and is 
regularly increased by exercise, so that the blood may be 
passed in considerable quantities. 

From time to time there occur acute exacerbations of the 
pyelitis. There may be an initial chill ; the temperature 
rises to 102° or 104° F. and is accompanied by severe 
and distressing pain in the back. Profuse sweating follows 
the decline of the fever. During the attack the urine 


664 MANUAL OF THE PRACTICE OF MEDICINE. 

becomes smoky or bloody and contains a large number of 
epithelial cells. This “ intermittent renal fever,” which may 
be mistaken for malarial fever, is identical with the inter¬ 
mittent hepatic fever due to gall-stones. 

Severe cases of pyelitis may merge into those of suppu¬ 
rative pyelo-nephritis and pyonephrosis. The symptoms of 
pyelitis become aggravated, pus appears in the urine, and 
chills, fever, and other septic symptoms develop. If the 
opposing kidney be previously destroyed by calculous dis¬ 
ease, pyelo-nephritis may lead to fatal uraemia. Other cases 
die in a septicaemic condition. 

Treatment should be directed toward the following con¬ 
ditions : 

1. The habitual passage of uric-acid or oxalate-of-lime 
crystals. Usually there is found some digestive error. 
The bowels should be kept regular; the functions of the 
liver should be stimulated by cholagogues and occasional 
doses of calomel. The use of dilute hydrochloric acid 
(ttlxv in a glass of water to be drunk during meals) is often 
of the greatest service, especially in cases of oxaluria. A 
reduction should be ordered in fats, sugars, alcohol, and 
meat, but fruits, vegetables, and milk may be given freely. 
The most important part of the treatment is to enforce 
regular and systematic exercise ; unless this can be done, 
the effects of dietetic and medicinal treatment may not be 
apparent. 

2. Attacks of renal colic. The indication is to relieve the 
pain and spasm. The patient should at once be immersed 
in a hot bath, or hot applications may be applied to the 
abdomen. Morphine is to be given in grain doses hypo¬ 
dermically, and is preferably combined with atropine. The 
same caution attends its use as in biliary colic. The pain 
having a tendency to cease suddenly, the tolerance for the 
drug will also cease, and toxic symptoms may appear if the 


AE PUR OLITHIASIS. 


665 


drug be given in too liberal doses. While the patient is 
passing under the effects of the morphine whiffs of chloro¬ 
form may be necessary to mitigate the agony. After the 
attack is over the urine for some days should be filtered 
through gauze or through a fine sieve to find the stone, and 
by analysis its chemical composition may be determined. 

3. If the stone be impacted in the ureter , treatment is 
given with a view to relax the spasm of the wall of the 
ureter, and to increase the quantity of urine, so as to push 
the stone along. 

Spasm is relaxed by continuous hot applications and hot 
baths, during which the abdomen may be kneaded gently, 
and by small doses of morphine and atropine. Increased 
secretion of urine is accomplished by raising the blood- 
tension by appropriate heart-stimulants, the preferable drug 
for this purpose being digitalis. 

If medicinal treatment be of no avail, and if anuria per¬ 
sist, showing permanent disability of the other kidney, the 
stone may be removed surgically. 

If the stone remain in the pelvis of the kidney, various 
forms of solvent treatment have been recommended. 
Citrate of potash is to be given in doses sufficient to keep 
the urine neutral in reaction. The treatment must be dis¬ 
continued as long as the urine is alkaline or ammoniacal. 
According to Roberts, three conditions are necessary for 
success in this treatment: the calculus must be of uric 
acid; it must be of small size; and the urine must not be 
alkaline or ammoniacal, as otherwise sodium biurate or 
phosphate is precipitated upon the calculus, rendering 
further solution impossible. 

Instead of the citrate of potassium, alkaline mineral 
waters may be given for the same purpose, but, according 
to Hai cr the lithium waters are useless. For the oxalate- 

o ’ 

of-lime calculi there is no solvent treatment. If the pain 


666 MANUAL OF THE PRACTICE OF MEDICINE. 


be so severe as to interfere with the patient’s earning a 
living, or if suppurative pyelo-nephritis or pyonephrosis 
develop, the kidney may be cut down upon and the calculi 
removed or the kidney extirpated. Care, however, should 
be taken that the other remaining kidney is competent, and 
not atrophied from previous disease or congenitally absent 

PERINEPHRITIC ABSCESS. 

Etiology. —Suppuration of the perinephritic tissues may 
result from traumatism or from extension of suppuration 
from the kidney, intestine (especially the vermiform appen¬ 
dix), liver, or spinal column. Burrowing downward of a 
perforating empyema has occurred. 

Symptoms.—As the disease is, properly speaking, a sur¬ 
gical one, but a brief description of the symptoms will be 
given. Pain and tenderness are present in the lumbar 
region. The pain is somewhat relieved by keeping the 
body immobile and by flexing the thigh. In rare cases the 
pain may be altogether referred to the hip-joint or to the 
knee. In the lumbar region there may be detected a 
tender, indurated mass which in the latter stages may yield 
a sense of fluctuation. The abscess may appear externally, 
or internal rupture in any direction may occur. 

The constitutional symptoms are those of an internal 
abscess—chills, fever, and the gradual development of 
sepsis. 

Treatment consists in opening and draining the abscess. 


VI. CONSTITUTIONAL DISEASES. 


ACUTE ARTICULAR RHEUMATISM; RHEUMATIC 

FEVER. 

Etiology. —Rheumatism may occur at any time of the 
year, but it is more common in the spring months. Hered¬ 
ity is traced in 25 per cent, of the cases. One attack pre¬ 
disposes to successive attacks, and relapses are common. 
No age is exempt. It is very common in children, and it 
may even be a disease of intra-uterine life. It occurs espe¬ 
cially in those leading a life of exposure, and the exciting 
cause may be wet and cold or over-strain of a muscle or a 
joint. The disease is rare in the tropics. 

Rheumatism at certain times assumes epidemic propor¬ 
tions, and when this is the case the clinical features are apt 
to vary. 

The following theories of rheumatism have been advanced; 
no one of them has been satisfactorily proven: 

1. The nervous theory , that rheumatism depends upon dis¬ 
turbances of the nerve-centres presiding over the nutrition 
of joints. 

2. The lactic-acid theory , that rheumatism is due to the 
presence of lactic acid in the blood, due to some perverted 
tissue-change of muscle. 

3. The uric-acid theory of Haig, that uric acid formed in 
the blood may be deposited in the joints by diminished 
alkalinity of the blood. It has been supposed that lactic 
and uric acid in combination might produce the lesions. 

667 



668 MANUAL OF THE PRACTICE OF MEDICINE. 

4. The theory of microbic infection is based upon the gen¬ 
eralization of the lesions, the involvement of the fibro-serous 
membranes so commonly involved in other known bacterial 
diseases, the constitutional predisposition seen in many 
patients, and the occurrence of occasional epidemics of the 
disease. No germ has yet been isolated, although ex¬ 
periments seem to confirm the theory of bacterial in¬ 
fection. 

Symptoms—1. General .—The onset may begin acutely 
with a chill and fever, or subacutely by shooting pains in 
the joints, malaise, and moderate fever. In rarer cases the 
joint-symptoms are the first symptoms observed. 

The fever is rarely intense, usually under 103° F., and 
runs no typical course. Formerly its duration was from 
two to four weeks, but owing to improved methods of treat¬ 
ment it now rarely lasts more than from two to five days. 
In children the fever is but moderate, and it may even be 
absent. It is important to watch the temperature through¬ 
out the disease. A rise in temperature usually means a 
fresh invasion of joints, or some complication, such as endo¬ 
carditis or pericarditis, while a fall generally implies a sub¬ 
sidence of the disease and modifies the therapy. The occur¬ 
rence of hyperpyrexia will be noted later. 

The pulse is full and dicrotic. 

The urine is diminished, is of increased acidity and high 
specific gravity, and contains urates and an increased quan¬ 
tity of uric acid. Febrile albuminuria may be observed. 

Cerebral symptoms are not seen except in cerebral rheu¬ 
matism with hyperpyrexia or in over-dosing of salicylic 
acid. 

The blood in rheumatism becomes rapidly anaemic. In 
the majority of cases there occur drenching sweats of a 
peculiarly sour odor, and the skin may show sudaminal 
vesicles. 


ACUTE ARTICULAR RHEUMATISM. 669 

2 . Inflammation of Fibro-serous Membranes .—The joints 
are almost regularly involved, giving a distinct clinical type 
to the disease. In children, however, joint-symptoms are 
regularly less marked than in adults, and may be absent 
altogether (the “ abarticular ” form). The lesion is a simple 
serous synovitis. The synovial membrane is hyperaemic; 
its cavity is filled with serum and flocculi of fibrin. There 
is no pus-formation. There are often similar lesions in the 
sheaths of adjacent tendons. There are pain, increased by 
motion, and tenderness of the affected joints. The extent 
and character of the swelling depend upon the amount of 
synovial effusion and the involvement of the adjacent ten¬ 
don-sheaths. The skin over the joint is usually hot, red¬ 
dened, and not infrequently is oedematous. These symp¬ 
toms are less marked in children, who may only show some 
rigidity to passive motion of the joint, and a continued posi¬ 
tion of flexion which is especially marked in the knees, 
and appears to be due to inflammation of the sheaths of the 
hamstring tendons, the joints themselves escaping. 

Characteristic of rheumatic synovitis are the great rapidity 
of its development and subsidence, the involvement of many 
joints by jumps (fresh articulations being involved while 
those first attacked are recovering), and the rarity of its 
attacking one joint alone. Monarticular rheumatism is so 
uncommon that a diagnosis of rheumatism should always 
be made with extreme caution. The larger joints are 
especially liable to be attacked, but the small joints of the 
hands and the feet may be involved. Any joint may be 
attacked, but the temporo-maxillary articulation is so rarely 
involved as to throw doubt on the diagnosis, should this 
joint be affected. Symmetry of involvement is rare, the 
disease differing in this respect from acute rheumatic arthri¬ 
tis. Pain and swelling often persist after the acute process 
has subsided, and there may be some stiffness from adhe- 


6 yO MANUAL OF THE PRACTICE OF MEDICINE . 


sions within the joint-cavity. An acute attack may be fol¬ 
lowed by any of the forms of subacute or chronic rheuma¬ 
tism. Recurrences of acute rheumatism are exceedingly 
common, especially in the rheumatism of young people. 

Subacute rheumatism represents a milder form of rheu¬ 
matism. The constitutional and local symptoms are less 
intense, but the duration of the disease is longer than in the 
acute form, and the condition tends to become chronic. 

Complications of Rheumatism.—i. Cardiac Affections. 
—The endocardium and the pericardium may be involved 
in mild as well as in severe attacks of rheumatism, and may 
even be inflamed without any involvement of the joints, as 
in the abarticular rheumatism of children. The liability to 
heart-complications is most common in children ; this liabil¬ 
ity diminishes with increasing age. The heart-membranes 
are not usually involved after the first week, if absolute rest 
and a restricted diet be enforced. 

(a) Pericarditis , which complicates from io to 20 per cent, 
of the cases, may occur alone or with endocarditis. The 
inflammation may be fibrinous, fibrino-serous, or purulent, 
and it is often associated with hyperpyrexia and delirium. 
The rheumatic pericarditis of children often runs an obscure 
course. The child grows pale and emaciated, and dies of 
exhaustion or of heart-failure without the development of 
either dropsy or dyspnoea. 

( b ) Endocarditis is more commonly a rheumatic lesion 
than pericarditis, and it appears in a large percentage of 
both mild and severe cases. Endocarditis may even be the 
solitary manifestation of the abarticular rheumatism of chil¬ 
dren. The mitral valve is the one most frequently affected. 
Valvular disease may not lead to serious consequences, or 
slow changes may ensue, resulting in valvular thickening 
and retraction. In a few cases there occurs an added infec¬ 
tion of micrococci, resulting in malignant endocarditis. 




ACUTE ARTICULAR RHEUMATISM. 67 I 

(V) Myocarditis is almost regularly secondary to endo¬ 
cardial or pericardial changes. 

2. Pulmonary Affections .—(<3) Pleurisy usually results by 
extension from a pericarditis, and is therefore left-sided and 
more intense in the portion of the pleura in most direct con¬ 
tact with the pericardium. The pleurisy is usually fibrinous, 
rarely fibrino-serous. 

(f?) Rheumatic pneumonia rarely occurs except in connec¬ 
tion with pericarditis, and is left-sided. The pneumonia 
may present certain peculiarities : (1) Absence of the criti¬ 
cal fall of temperature; (2) frequent absence of cough; (3) 
rarity of rusty sputum ; (4) great rapidity with which the 
physical signs clear up. 

3. Hyperpyrexia is probably due to the action of the 
rheumatic poison upon the heart-centres, and is of compara¬ 
tively rare occurrence. It appears more commonly in hot 
weather; it is more frequent in men than in women, and 
especially in those with weak nervous systems. It is un¬ 
known in childhood, the greatest liability being between the 
twentieth and thirtieth years. It is almost unknown after 
the third attack of rheumatism. In one-half the cases peri¬ 
carditis is present. In an equal number of cases the joint- 
symptoms subside as the hyperpyrexia develops. The 
hyperpyrexia may complicate mild or severe cases. The 
onset of high fever may be sudden, or it may be preceded 
by headache, delirium at night (not due to salicylic acid), 
restlessness, hyperaesthesia of the skin, or excessive mictu¬ 
rition. The fever may rise gradually or suddenly to 106°, 
108 0 , or 110° F., or there may be merely a high range of 
temperature for a number of days, without any acute exacer¬ 
bation. Prostration, delirium, and coma usually appear, and 
may terminate fatally. 

4. Cerebral complications complicate the hyperpyrexia, 
and occur only in about 2 per cent, of the cases. Cerebral 


672 MANUAL OF THE PRACTICE OF MEDICINE. 

symptoms may suddenly develop, or they may be preceded 
by the same prodromal symptoms as in hyperpyrexia. 
These preliminary symptoms, if proven not to be due 
to salicylic-acid poisoning, should excite grave appre¬ 
hensions. 

According to Duckworth, cerebral rheumatism assumes 
one of three clinical types : 

(a) There is delirium, mild and wandering or so violent as 
to call for restraint, followed by semi-coma, coma, and 
death. 

(b) The patient passes suddenly into coma, which termi¬ 
nates fatally, at times within a few hours. 

(,:) There are well-marked spasmodic symptoms, followed 

by fatal coma. 

In the great majority of the cases of cerebral rheumatism 
hyperpyrexia is present, and if the temperature be over 106° 
F., a fatal issue is almost certain unless prompt treatment 

be adopted. 

The pathology of cerebral rheumatism is obscure. The 
brain may be normal, anaemic, or congested. In rare 
instances there are found evidences of an acute meningitis. 

5. The relation of chorea to rheumatism will be con¬ 
sidered under the former disease. 

6. Cutaneous Complications .—There may be a fine miliary 
rash, or an eruption resembling that of scarlet fevei. Pui- 
pura is not uncommon, and the various forms of urticaria 
and erythema may occur. 

7. Rheumatic Nodules .—Subcutaneous nodules, varying 
from a barely appreciable size up to that of a bean, may 
appear, attached to the tendon-sheaths, to the deep fascia 
covering the bony prominences, and to the cranium. Those 
attached to the tendon-sheaths are freely movable. During 
the early stages of their development they may be a little 
tender, but when of longer duration they aie absolutely 


A CUTE A R TICUL A R RUE UAL V TTSM. 


673 


painless. They are most numerous on the fingers, the 
hands, the wrists, and about the elbow-joints, but they may 
appear upon the patellae, the spines of the vertebrae, the skull, 
and the clavicles. They may appear during an attack of 
rheumatism or after its decline, and they are more common 
in the abarticular rheumatism of children. They may last 
for weeks or months, and they are regarded as a positive 
indication of rheumatism. They consist of connective tissue 
undergoing rapid proliferation. 

8 . Pharyngitis and Tonsillitis.—Pharyngitis is not uncom¬ 
mon in rheumatic subjects, and is characterized by the 
amount of pain being out of proportion to the apparent 
degree of inflammation. Rheumatic pharyngitis may be 
practically considered as an erythematous affection of the 
fauces, of a nature similar to cutaneous erythema. 

Tonsillitis occurs in repeated attacks in rheumatic sub¬ 
jects, and may complicate an acute rheumatic attack. 

Treatment.— Except in very subacute cases, the patient 
should be put to bed, no matter how mild the case, and not 
be allowed to get up until the acute symptoms have entirely 
subsided. The diet should be of milk and farinaceous food, 
nitrogenous food being absolutely contraindicated. Lemon¬ 
ade or the alkaline mineral waters may be given freely. 
The patient should not be exposed to draughts, and should 
sleep between light blankets. 

Local treatment to the affected joints is often grateful. 
The joints may be encased in cotton and rendered immobile 
by padded splints. Hot applications are usually well borne, 
hot solutions of 1 per cent, of acetate of alumina or of lead 
and opium being highly efficacious. Counter-irritation by 
the thermo-cautery or by small blisters about the joint 
sometimes relieves the pain. The joints may be bathed 
with chloroform liniment, or ichthyol ointment ($j: ,$j) may 
be applied. Ice-bags are at times more grateful than hot 
43 


6/4 MANUAL OF THE PRACTICE OF MEDICINE. 

applications, and are much used on the Continent of 
Europe. 

Constitutional Treatment .—Salicylic acid (gr. v-x), sodium 
salicylate (gr. x-xx), salol (gr. v-x), salophen (gr. v-x), and 
oil of wintergreen (TH x-xx in capsule or in milk) may be 
eiven in the indicated doses every two hours until slight 
deafness and buzzing noises in the ears are experienced, 
after which the dosage is to be reduced gradually. This 
salicylic-acid treatment seems to have no effect in redu¬ 
cing the duration of the disease nor in preventing cardiac 
complications, but it exerts a specific effect upon the fever 
and the pain, the temperature falling to normal and the 
articular pains disappearing within from two to five days. 
It is said that relapses are more common under this than 
under the alkaline treatment, but the so-called “ relapses ” 
are probably recrudescences of the disease, as the symp¬ 
toms of rheumatism tend to recur should the treatment be 
discontinued too soon or should too small doses of the 
salicylic acid be given. Toxic symptoms—gastric disturb¬ 
ances, delirium, cardiac weakness, albuminuria, and a tend¬ 
ency toward hemorrhages—should not appear if the patient 
be conscientiously watched. 

The alkaline treatment seems to lessen the liability to 
cardiac complications. The treatment consists in giving 
alkalies in dose sufficient to keep the urine alkaline. For 
this purpose sodium bicarbonate in 3 j—ij doses should be 
given every three hours, in water rendered effervescent by 
the addition of the juice of half a lemon. The urine 
becomes alkaline usually within twenty-four hours, after 
which time only enough alkali is given to keep the alkalin¬ 
ity of the urine constant. The addition of quinine sulphate 
(gr. iij-v) to each dose of the alkali seems to increase its 
therapeutic value. The alkaline treatment may be given 
alone, but it is preferably combined with the salicyl com- 


CHRONIC ARTICULAR RHEUMATISM. 675 

pounds. Trimethylamine and benzoic acid or sodium 
benzoate have been recommended for rheumatism, but their 
action is inferior to that of the salicylates. 

For the relief of pain opium may be necessary. Phen- 
acetine is of service, and antipyrine, in 10-grain doses every 
three or four hours, is useful in controlling the pains of 
afebrile rheumatism. 

Hyperpyrexia is to be treated by the energetic use of the 
wet pack or the cold bath, and no time should be lost in 
reducing the temperature. 

The treatment of the cardiac and pulmonary complica¬ 
tions is considered under their respective sections. 

During convalescence iron is indicated to relieve anaemia, 
and the alkaline treatment should be continued for some 
weeks after the cessation of acute symptoms. Over-use 
of the joints should be avoided. During convalescence 
nitrogenous food should be interdicted. 

PSEUDO-RHEUMATISM (SECONDARY 
RHEUMATISM). 

Under this heading are included a number of forms of 
articular disease secondary to a variety of infectious 
diseases, usually of septic origin. Among the most com¬ 
mon of these diseases are the articular affections complicat¬ 
ing mumps, dysentery, scarlet fever, typhoid fever, puer¬ 
peral fever, pyaemia, purpura rheumatica, syphilis, and 
gonorrhoea. The characteristics of these pseudo-rheu¬ 
matic affections will be considered in connection with 
the diseases from which they originate. 

CHRONIC ARTICULAR RHEUMATISM. 

Etiology. —The chronic form may follow acute rheumatism, 
or the disease may be chronic from the start. Persons past the 
middle age of life, and whose occupation exposes them to 


676 MANUAL OF THE PRACTICE OF MEDICINE , 

wet and cold, are more liable to be attacked. The disease 
is greatly influenced by weather, and exacerbations may 
recur every autumn and last throughout the winter. 

Pathology. —The synovial membrane is congested, and, 
together with the capsule of the joint, is thickened. The 
thickening may also extend to the fibrous structures about 
the joint. Slight erosions of the articular cartilages may 
occur in protracted cases. There may be deformities from 
the contraction of fibrous bands formed about the diseased 
joints (rheumatisme fibreux ), and in advanced cases ankylo¬ 
sis of the joint may occur. There may be atrophy of the 
muscles about the diseased joint, from disuse, from centric 
nervous causes, or from neuritis. Muscular contraction is 
not uncommon. Osteophytic deposits do not occur as in 
arthritis deformans. There are no cardiac complications 
as in the acute form. 

Symptoms. —Pain and stiffness characterize the affected 
joints, and acute exacerbations may occur, especially after 
over-exertion of the joints or during cold, damp weather. 
The affected joints are tender to the touch and are usually 
somewhat swollen. Synovial crackling may be appreciated 
on movement, and may readily be distinguished Irom the 
bony grating common to anthritis deformans. As a rule, 
many joints are involved, especially those exposed to fatigue 
in the patient’s ordinary occupation. In working-women 
the small joints of the hand are usually favorite seats of the 
disease. Ulnar deflection of the fingers is common, but the 
deflection is not permanent except in the fibrous or ankylotic 
form. In rare cases the disease assumes a monarticular 
form, involving the hip, the knee, or the shoulder. The 
course of the disease is afebrile, and the general health does 
not directly suffer from the disease. 

The prognosis is good for life, but is bad for recovery 
from the rheumatism. 


MUSCULAR RHE UMA TISM. 


6/7 

Treatment.—The clothing should be warm, and exposure 
to cold, damp weather should be avoided. Salicylic acid is 
useless. A number of drugs have been recommended for 
this disease—potassium iodide, colchicum, arsenic, alkalies, 
guaiac, preferably combined with potassium citrate and 
tincture of cinchona—but the efficacy of internal treatment 
can seldom be demonstrated. Good results have been 
claimed for ichthyol (gr. v three times a day in pill form). 
The best results are obtained by improving the patient’s 
nutrition (tonics, nutritious food, and cod-liver oil), by ap¬ 
plying counter-irritation to the joints (thermo-cautery, iodine, 
blisters), and by sending the patient for the winter months to 
a warm, equable climate. Hot alkaline waters are particu¬ 
larly useful, and sulphur-waters have also been recom¬ 
mended. The thermal springs may be advised, together 
with a change of climate. Alkaline baths have been recom¬ 
mended, but they are not to be advised in the case of those 
over sixty years of age with atheroma and myocardial 
degeneration. 


MUSCULAR RHEUMATISM. 

Etiology. —The exact nature of this affection is unknown. 
The condition, which commonly occurs after exposure to 
cold and after over-use of the muscles, is more frequent in 
those of a rheumatic or gouty habit. One attack renders 
the patient susceptible to recurrences. 

The pathology is unknown. The disease may be a mild 
form of inflammation of the muscles (myositis), or the affec¬ 
tion may be entirely neuralgic. 

Symptoms.—There is pain, dull and aching or sharp 
and cramp-like, in the affected muscles, and the pain is 
regularly increased by motion. The pain is generally re¬ 
lieved by pressure, but there may be decided muscular ten¬ 
derness. The affected muscles may be contracted, so that 


678 MANUAL OF THE PRACTICE OF MEDICINE . 

the attitude of the patient frequently gives evidence as to 
the seat of the disease. Special names are given to muscu¬ 
lar rheumatism according to the location of the difficulty. 
Lumbago affects the muscles of the small of the back and 
their tendinous attachments. Torticollis , or “ wry-neck,” 
usually affects the sterno-cleido-mastoid muscle of one side, 
but both muscles may be affected, and the muscles of the 
back of the neck are often involved. Pleurodynia involves 
the intercostal muscles of one side, and occasionally the 
pectorals, the latissimus dorsi, and the serratus magnus. 

The duration of muscular rheumatism is usually brief, but 
the disease may at times run a subacute or a chronic course. 

Treatment.—Rest for the affected muscles is of the first 
importance. As the pain begins to wear away, the sub¬ 
sidence of the disease may be hastened by massage. In 
some cases massage will cut short a pronounced attack, and 
the effects of the manipulations may be increased by the use 
of stimulating liniments. Strapping of the side gives relief 
in pleurodynia. Phenacetine combined with salol or with 
salicylic acid frequently cuts short an attack, and should 
always be used as routine treatment. Steaming by covering 
the affected muscles with damp cloths and passing a hot 
iron over them is a domestic remedy of established value. 

A hot bath may be recommended. Rapid cure frequently 
follows “ firing ” with the thermo-cautery. The use of the 
constant current is also beneficial. Osier recommends acu¬ 
puncture for lumbago, sterilized bonnet-needles three or 
four inches long being thrust into the affected muscles and 
retained from five to ten minutes. In many cases instant 
relief follows this procedure. 

GOUT (PODAGRA). 

Etiology.—Gout may be either inherited or acquired. 
Inherited gout is very common among the better classes in 


GOUT. 


679 


England, Germany, and France, but is rare among the Irish. 
An inherited tendency is seen in 75 per cent, of the cases. 
Gout may be acquired by habits of ease, indolence, and dis¬ 
sipation, by over-eating and over-indulgence in alcohol, by 
deficient bodily exercise, and by any cause exhausting the 
great nerve-centres. It may be acquired through poisoning 
by lead, as Garrod found that 30 per cent, of his hospital 
cases of gout could be traced to this origin. Gout cannot 
always be traced to high living, as cases of “ poor man’s 
gout” are not uncommon, the disease being induced by 
improper hygiene, poor food, and indulgence in malt liquors. 
In America the acute forms of gout are uncommon, but the 
irregular manifestations of the disease are not infrequent. 
The disease occurs more often in men than in women. The 
inherited form usually appears earlier in life than the ac¬ 
quired form, which does not generally appear until the fifth 
decade. 

Three theories of gout have been advanced: 

1. The Uric-acid Theory (Garrod).—From renal insuffi¬ 
ciency the excretion of uric acid is diminished, and the 
symptoms of gout arise from its retention in the blood and 
tissues and from the efforts of nature to expel it. The de¬ 
posit of crystallized urates in the joints gives rise to the 
classical inflammatory symptoms. Haig has thus modified 
the uric-acid theory: The deposit of urates, according to 
his modification, is not due to their excessive production 
nor to deficient elimination, but is produced by all conditions 
associated with diminished alkalescence of the blood. 

2. The “Nervous” or “ Nervo-humoral” Theory (Duck- 
wor th).—Two conditions must be complied with: (1) The 
patient must possess the arthritic or diathetic habit from 
which gout and rheumatism arise, and (2) there must exist 
some functional disturbance of the nerve-centres to account 
for the sudden explosion of the symptoms. This “ gouty 


680 MANUAL OF THE PRACTICE OF MEDICINE. 

neurosis ” may be inherited, acquired, intensified, or re¬ 
pressed. The causative effect of depressing physical and 
mental circumstances in inducing gout seems to lend cor¬ 
roboration to the nervous theory. 

3. Ebstein believes that a local necrosis occurs in certain 
tissues from local nutritive disturbance, and that in the 
necrotic areas the urates are deposited secondarily. The 
nutritive-tissue disturbance may be inherited or acquired. 

Pathology.—The blood contains an excess of uric acid. 
This condition, however, also occurs in leukaemia, and is not 
therefore distinctive. The joints usually affected are the 
great toe, the small joints of the hands and the feet, and, 
least frequently, larger joints without any marked order of 
preference. During an acute attack the synovial membrane 
is congested, the ligaments are swollen, and there is an in¬ 
crease in the synovial fluid. The articular cartilages appear 
as if whitewashed, from an interstitial deposit of the sodium 
urate, with occasionally the addition of the calcium salt. In 
advanced cases the cartilage becomes roughened and eroded 
and infiltrated with urates, while deposits of urates are seen 
in the ligaments and in the neighboring fibrous structures. 
The synovial fluid is often transformed to a pasty mass of 
urates. 

Secondary inflammatory lesions consist of bony marginal 
outgrowths, and in ulceration by which the gouty masses 
may be discharged through the skin. The joint becomes 
distorted and immobile, and complete ankylosis may result. 
Gouty concretions or “ tophi ” are frequently seen under 
the skin, in the eyelids and the ears, and in other parts of 
the body. 

Associated lesions are of great importance. 

I. The kidneys may show deposits of sodium urate as 
whitish lines in the apices of the pyramids. Chronic diffuse 
nephritis is so commonly present that the name “ gout}’ 


CoVT. 681 

kidney has frequently been applied to this form of 
nephritis. 

2. The arteries are frequently the seat of chronic endar¬ 
teritis. Atheroma and calcareous deposits upon the aortic 
valves are not infrequent. 

3. Hypertrophy and dilatation of the heart result from 
the nephritis, from the endarteritis, and from the atheroma 
of the aortic valves. 

4. Emphysema with chronic bronchitis is almost con¬ 
stantly present in the chronic forms of gout. 

5. Chronic gastro-enteritis or chronic colitis is frequent 
in long-standing cases. 

Symptoms.— Gout may be described as occurring in 
acute, chronic, and irregular forms. 

Acute Gout.— There may be premonitions of an attack. 
These premonitions consist of twinges of pain, cramps in 
the calves, irritability of temper, and dyspepsia. A pre¬ 
liminary asthmatic attack may also occur. The urine is 
usually over-acid and concentrated, and deposits urates. 
There may be a temporary albuminuria or glycosuria. The 
quantity of uric acid eliminated before and during the early 
period of the attack is regularly diminished. The attack 
itself generally appears suddenly, usually during the early 
morning hours, with a characteristic pain in the metatarso¬ 
phalangeal joint of the great toe, usually of the left side. 
The pain is grinding, throbbing, and excruciating, and is 
entirely disproportionate to the evident inflammation. The 
joint becomes swollen, dusky-red, shiny, and tender. The 
veins of the foot become turgid. As the attack wears off 
the foot usually becomes cedematous, and desquamation of 
the skin over the joint is observed. An initial chill is not 
uncommon. Fever amounting to 102° or 103° F. is almost 
regularly observed. 

Other joints may become involved, especially the joint 


682 MANUAL OF THE PRACTICE OF MEDICINE. 

of the great toe of the other foot, but this extension of 
the disease is not common. A practical rule is that all 
cases of suddenly induced severe monarthritis should be 
suspected to be of gouty origin. In rarer cases the knee- 
joint is the one primarily involved. 

The attack terminates favorably within a week or ten 
days, unless the response to treatment be exceedingly 
prompt, and the patient is left with a weakened, tender 
joint for some little time. Usually, after an acute attack 
the general health is markedly improved. 

The terms “ suppressed ” and “ metastatic ” gout are ap¬ 
plied to sudden and severe internal symptoms coincident 
with the rapid disappearance of the outward inflammatory 
signs. The following varieties may be described : 

1. Cardiac gout consists of sudden pain in the heart, syn¬ 
cope, and heart failure which may be fatal. If the patient 
recover, dyspnoea and palpitation appear. 

2. Cerebral Gout. — There may be mental confusion, 
delirium, or mania. Apoplectiform seizures with coma 
may occur. Temporary insanity has been observed. In 
some of these cases, however, the cerebral symptoms have 
been uraemic. 

3. Gastro-intestinal Gout. —Pain in the stomach, nausea, 
and vomiting are not infrequent. Profuse diarrhoea may 
occur, with death in collapse. 

4. Vesical gout is characterized by frequent painful mic¬ 
turition and haematuria. 

5. Testicular gout is accompanied by painful swelling of 
the testis. 

Chronic Gout. —As the acute attacks become more fre¬ 
quent the local processes fail to leave the joints. The joints 
show various deformities, depending on the bony out¬ 
growths from the periphery of the articular cartilages, from 
visible deposit of urates, and from enlargement of and gouty 


GOUT. 


683 

deposits in the superjacent bursae. Synovial distention is 
less common in gout than in rheumatism. Crackling 
sounds are heard when the joints are moved. Pain and 
weakness are experienced in the affected joints, which first 
are those of the feet, then those of the hands. Tophi 
appeal about the joints and in the ears, and mav be dis¬ 
charged through the skin. The skin becomes soft and 
satin-like. Symptoms of the associated lesions appear— 
high-tension pulse from the arterial changes, hypertrophy 
or dilatation of the left ventricle, abundant urine of low 
specific giavity, and uraemic symptoms from the nephritis. 
Emphysema, bionchitis, and chronic intestinal catarrh com¬ 
plicate the course of the disease in almost all cases. 

Irregular 01 abarticular gout is extremely common, 
occurring as an inherited and as an acquired form. Various 
symptoms appear in different members of gouty families 
and among those whose habits are such as to predispose to 
gout. The symptoms are so varied and assorted that only 
a brief mention can be made of the most important: 

1. Cutaneous Symptoms .—Eczema is frequent, especially 
the dry, scaly variety. Pruritus ani and hot itching feet 
at night are commonly the source of much distress. 

2. Gastro-intestinal Symptoms .— Dyspepsia is the rule. 
Flatulence, over-acidity, constipation, coated tongue, “ bil¬ 
iousness,” and the symptoms of functional disturbance of 
the liver are usually present. 

3. Urinary Symptoms .—The urine is usually over-acid 
and deposits urates, uric acid, and lime oxalate. Temporary 
glycosuria and albuminuria are not uncommon, especially 
in patients of advanced years. The symptoms of chronic 
diffuse nephritis without exudation may appear. Renal 
calculi are not uncommon, and are usually of the uric-acid 
variety. Urethritis may develop without gonorrhoeal in¬ 
fection. 


684 manual of the practice of medicine. 

4. Cerebral symptoms are not uncommonly distressing. 
They comprise mental hebetude, loss of memory, irritability 
of temper, headaches of such severity as to suggest organic 
disease, vertigo, and sleeplessness. The eyesight is com¬ 
monly blurred, and the eyeballs may be hot and itching. 

5. Cardio-vascular Symptoms. — Vaso-motor symptoms 
are common, and consist of “ hot and cold flushes and 
sudden sweatings. The pulse is one of high tension. 
Palpitation is a common symptom. The arterial changes 
may lead to the symptoms of hypertrophied or dilated 
heart, atheroma of the aorta or of the coronary vessels, 

aneurysm, or sudden death. 

6. Pulmonary symptoms include chronic bronchitis, em¬ 
physema, and asthmatic attacks. 

7. Locomotor Organs. —Shooting pains, stiffness, and sub- 
tendinal bursitis are common. Cramps in the calves of the 
legs, burning feelings in the feet at night, and tenderness in 
the heels on standing may appear. Gouty neuralgia is not 
infrequent, and involves the sciatic nerve with greatest 
frequency. 

8. Eye-affections. —A number of conditions may occur, 
among which iritis and glaucoma are the most important. 
Conjunctivitis is not uncommon, and may be due to gouty 
tophi in the upper lid. 

Prognosis.—Gout is seldom the actual cause of death 
except in the rare visceral forms; but the disease is ren¬ 
dered serious by reason of the nephritis and the arterial 
sclerosis which so frequently complicate the disease, and it 
is upon these latter conditions that the prognosis depends. 

Treatment.—During an acute attack of gout the foot 
should be elevated and wrapped in cotton. Hot applica¬ 
tions are often of service, hot whiskey and water being a 
favorite application. Menthol may be used in alcoholic 
solution. The following prescription is used by Duckworth: 


GOUT. 


685 


^ Atropinae, g r . iij; 

Morphinae hydrochloratis, gr. xv ; 

Acidi oleici, gj.—M. 

Sig. Paint over painful joint with a camel’s-hair brush. 

Colchicum has a specific effect on acute gout, and the wine 
or the tincture should be given in doses of from 15 to 20 
minims every four hours, preferably combined with potas¬ 
sium citrate. A preliminary mercurial purge is usually 
given with advantage. The administration of colchicum 
should be watched carefully, and gastric distress and pur¬ 
gation should be avoided. In cases where colchicum fails 
or is not well borne, potassium citrate or acetate in 20- to 30- 
grain doses may be given every two hours, combined with 
diluent drinks. The preparations of salicylic acid are often 
employed, but their action is inferior to that of colchicum. 
Phenacetine or chloral hydrate may be given for the relief 
of the pain, but morphine is to be used with extreme cau¬ 
tion. The diet during the acute attack should consist 
largely of milk and light farinaceous foods, and alcohol 
should be withdrawn unless especially indicated as a stimu¬ 
lant. 

The treatment of chronic and irregular gout is largely by 
diet and hygiene. Starchy and saccharine food should be 
avoided ; beer and wines should be prohibited absolutely. 
Lean meats, eggs, fish, green vegetables, and milk should 
constitute the principal portions of the diet. Sweet fruits, 
berries, melons, and bananas are to be omitted from the 
dietary, but oranges and lemons may be allowed. The food 
should be simple, wholesome, and indulged in with modera¬ 
tion. If stimulants are needed, whiskey with water is the 
least injurious form. The patient should drink freely of 
pure water or of any of the alkaline mineral waters. 

Hygienic treatment consists of daily baths with friction 


686 MANUAL OF THE PRACTICE OF MEDICINE. 


of the skin and regular systematic exercise. Exercise is 
one of the most satisfactory means of treating irregular 
gout, but it should not be carried to the point of fatigue. 

The medicinal treatment is symptomatic. Lithia-vvater 
is of great service. An artificial lithia-vvater can be made 
by dissolving a 3-grain tablet of effervescing lithium citrate 
in each glass of table-water that is taken throughout the 
day. Constipation is relieved by occasional mercurial pur¬ 
gatives and by the steady use of podophyllin and rhubarb. 
Small doses of colchicum (TTLv-x of the wine) with 10 
grains of potassium iodide are of service during the more 
active manifestations of the disease. Quinine, guaiac, and 
the benzoates are also recommended. Iron and arsenic 
should be given for anaemic conditions. In obstinate cases 
much good is derived from a course of treatment at medici¬ 
nal springs, such as the White Sulphur Springs or those at 
Saratoga, Carlsbad, Kissingen, or Homburg. The effects 
of the treatment are largely due to the improved dietetic 
and hygienic conditions that attend a course of treatment at 
these places. 


ARTHRITIS DEFORMANS. 

Etiology and Synonyms.—This disease may be primary 
in its origin, or it may follow rheumatism, gout, or gonor¬ 
rhoeal arthritis; 85 per cent, of the cases occur in women, 
especially in those at the time of the menopause. The 
influence of heredity is often marked, especially among 
the female members of a gouty family. Rarely the disease 
may occur in children. The true nature of the disease is 
obscure, but it seems probable that there is a nervous 
origin. This neuropathic theory is based upon the disease 
frequently following depressing nervous or mental shocks, 
upon the extreme symmetry of the lesions, and upon the 
atrophic changes occurring in the nails, the skin, and the 


ARTHRITIS DEFORMANS. 


687 


muscles. In many respects the lesions resemble the arthro¬ 
pathies of locomotor ataxia. Synonyms: Rheumatoid 
arthritis; Rheumatic gout. 

Pathology.—The joint-cartilage becomes fibrillated, soft, 
and velvety, and is worn away in the centre, exposing 
thickened, polished, eburnated bone-surfaces. At the periph¬ 
ery of the cartilages a lipping or a heaping up is observed, 
from which bony outgrowths form—the osteophytes. Im¬ 
mobility and deformity result from the interlocking and 
mutual obstruction of these osteophytes, but bony ankylosis 
does not occur except in the spinal column. The synovial 
membrane and the fibrous capsule become greatly thickened. 
Synovial distention is rarely extreme. Ligaments which 
pass in or through the diseased joints may be absorbed. In 
some cases the articular ends of the bones may be increased 
in length and thickness, but in old people the bones may 
become atrophied and spongy. Atrophic changes occur 
about the affected joints; the muscles undergo atrophy, the 
nails become brittle, the skin assumes a glossy appearance, 
and neuritis can frequently be demonstrated. 

Symptoms.—Three clinical types of the disease may be 
described: 

1. Heberderis Nodes .—The lesions involve the phalan¬ 
geal joints, and little nodules (Heberden’s nodes) develop 
on the distal phalanges. These nodes are composed of 
osteophytic outgrowths, and may show small cystic swell¬ 
ings at their summits, due to hernia of the joint-capsule. 
The joints may be swollen and painful after indiscretions in 
diet or when they are accidentally struck, but usually the 
chief symptom is limitation of motion. The phalangeal 
joints are somewhat enlarged, and may yield a bony 
grating on passive motion. The affection is incurable, but 
does not tend to advance. 

2. The Polyarticular Form .—This form may develop 


688 MANUAL OF THE PRACTICE OF MEDICINE. 


acutely and may be mistaken for acute articular rheumatism. 
It may be distinguished from the latter disease, however, 
by the symmetrical involvement of the small peripheral 
joints, by bony outgrowths from the articular ends of the 
bones, and by the uselessness of salicylic acid. The acute 
form of onset is most frequent in young women who have 
recently borne children. 

In other cases the onset is subacute. 

The chronic form is the most frequent. Premonitory 
symptoms are at times observed numbness and tingling 
of the skin over joints, rapid and high-tension pulse, and a 
persistent pain in the ball of the thumb. The small periph¬ 
eral joints are usually the first involved, and the lesions 
tend to advance steadily toward the trunk. The temporo- 
maxillary articulation is often involved. A characteristic 
feature is the extreme symmetry seen in the distribution of 
the lesion, for not only are corresponding joints simultane¬ 
ously involved, but the lesions progress in them with identi¬ 
cal rapidity. The joint-symptoms consist of pain, swelling, 
and limitation of motion. Pain is variable : it may be paiox- 
ysmal or of a steady, gnawing character, increased by mo¬ 
tion and by warmth in bed, or there may be neuralgic pain 
or the pain of muscular cramp. The enlargement of the 
joints is due to thickening of the capsule, to bony out¬ 
growths, and in some cases to synovial distention. Bony 
crepitus can usually be excited by passive motion. In time 
the joints become completely locked and immobile. De¬ 
formities are caused not only by distortion by the osteo¬ 
phytes, but also by muscular atrophy and spasm. The 
tendon-reflexes are usually increased, and ankle-clonus may 
be present. 

3. The Monarticular Form .—This form is most frequent 
in old people and in men. The hip, the knee, the shoulder, 
and the spinal column are the parts usually affected. In 


DIABETES MELLITUS. 


689 


many cases there is a history of previous joint-injury. In 
old people especially a slight injury is often sufficient to set 
up what may be regarded as a senile change. The lesions 
are essentially those previously described, but great atrophy 
of the ends of the affected bones is characteristic of the 
disease in old people. 

When affecting the hip-joint of the aged, the disease has 
been termed “ morbus coxae senilis.” Pain, limitation of 
motion, bony grating, and shortening are observed. The 
gluteal region is flattened from muscular atrophy. 

When affecting the spinal column, the disease has been 
termed “ spondylitis deformans.” Bony ankylosis is com¬ 
mon, so that immobility of the vertebral column in the in¬ 
volved section results. 

The prognosis is bad for recovery, although life is usually 
not shortened by the disease. Death occurs from intercur¬ 
rent disease, from chronic nephritis, or from tuberculosis. 
The disease may be arrested at any stage, or it may progress 
so that the patient is practically crippled. 

Treatment.—Arthritis deformans is practically an incur¬ 
able disease. Much good can be done, however, by build- 
ing up the general health and by the steady administra¬ 
tion of arsenic. A temporary improvement may follow 
prolonged treatment by hot mineral baths or by drinking 
the waters of thermal springs. Massage may be of service 
in preventing the muscular atrophy of disease. 


DIABETES MELLITUS. 

The term “diabetes” should be limited to those cases in 
which sugar accumulates in the blood and is excreted in the 
urine, accompanied by constitutional symptoms. The term 
“glycosuria ” should be applied only to those cases in which 
sugar appears in the urine in small amounts without consti- 
44 


690 MANUAL OF THE PRACTICE OF MEDICINE. 

tutional symptoms, or appears only as a temporary condi¬ 
tion. 

Etiology. —The disease may be induced by long-continued 
indulgence in saccharine food, especially if the patient be of 
sedentary habits. In many cases the influence of heredity 
is marked. The disease may follow lesions or injuries of 
the brain or of the spinal cord, and it has been produced 
artificially by puncture of the floor of the fourth ventricle just 
behind the pneumogastric nucleus (Bernard’s diabetic cen¬ 
tre). Lesions causing atrophy in extensive disease of the 
pancreas have been followed so frequently by diabetes that 
a special form of “ pancreatic diabetes ” has been described. 
Psychical disturbances, such as worry, care, and depressing 
emotions, have been followed by the disease, and in some 
cases diabetes has succeeded certain infectious diseases, such 
as syphilis, gout, and malaria. Disturbances of the liver 
have also been adduced as causative factors. The disease 
is not as common in America as on the Continent of 
Plurope. Men are more frequently attacked than women, 
and the greatest liability occurs in adult life. Children 
under ten years of age are usually exempt. Hebrews seem 
to be predisposed to diabetes, and the disease is more com¬ 
mon among the higher classes. 

To explain the disease a number of theories have been 
advanced. Nervous lesions, diseases of the pancreas and the 
liver, insufficient alkalescence of the blood-plasma, and de¬ 
ficient oxidation-processes have each been the subject of 
separate hypotheses, but no one theory has been established 
definitely. 

Pathology. —A number of different lesions have been 
found, no one of which seems to be either constant or 
essential. They may be thus classified: 

1. The blood contains an excess of urea, fat, and sugar. 
The fat-particles may be visible in coagulated blood; the 


DIABETES MELLITUS. 


691 


sugar may be raised from the normal 0.15 per cent, to 
0.40 per cent.; glycogen may be found within the leuco¬ 
cytes. 

2. Nervous System. —There may be tumors or cysts in¬ 
volving the “ diabetic centre ” in the medulla or involving 
the cerebrum. Anaemia, oedema, or atrophy of the cortical 
convolutions may be found, or congestion and thickening 
of the meninges. Perivascular changes in the brain and 
the cord may occur. There may be found a tumor press¬ 
ing on the vagus. Peripheral neuritis is not uncommon. 
The sympathetic ganglia may be enlarged. 

3. Cardio-vascidar System. —The heart may be fatty or 
enlarged. Hypertrophy is not uncommon, and dilatation 
may be the cause of death. Endarteritis is frequently 
observed. Endocarditis may result from the irritation of 
the endocardium by the sugary blood. 

4. The liver may be fatty or may be the seat of cirrhotic 
change. A peculiar form of pigmentary degeneration is 
described. 

5. The pancreas may be firm and atrophied, may be the 
seat of pigmentary cirrhosis, or may be the seat of cancer, 
of cysts, or of fat-necrosis. 

6. The kidneys are usually fatty. Glycogen is often 
found in the epithelium of Henle’s tubes. Chronic ne¬ 
phritis is common. 

7. The lungs frequently show the lesions of broncho¬ 
pneumonia or of lobar pneumonia. Gangrene may occur. 
The lungs of diabetics are frequently the seat of tubercular 
inflammation. 

8. The mucous membranes are usually the seat of chronic 
catarrhal inflammation. 

The symptoms of diabetes mellitus begin insidiously. 
The first symptom noticed may be an unnatural thirst, the 
passage of too much urine, or a loss of flesh. In some 


692 manual of the practice of medicine. 

cases the disease is first appreciated by an accidental exam¬ 
ination of the urine. In rare instances it sets in rapidly. 
When the disease is developed the symptoms are changes 
in the urine, thirst, hunger, progressive emaciation, and the 
symptoms due to the complications. 

i. The urine is usually pale, of a sweetish odor and taste, 
and is of a specific gravity ranging between 1025 and 1045, 
although a lower specific gravity may occur if the quantity 
of urine be enormously increased. The acidity is high. 
The urine irritates the genitals, causing intense pruritus, 
which may be the first symptom for which the patient 
applies for relief. Urea and phosphates are passed in 
excess, and acetone may be detected. A special form of 
diabetes has been described, “ phosphatic diabetes (Ralfe), 
in which phosphates are greatly increased, although the 
sugar may not be present constantly. Transient albuminuria 
is observed in about one-third of the cases. The quantity 
of urine passed varies between two and fifteen quarts, from 
four to six quarts being the quantity in average cases. In 
rare instances polyuria is not observed. The percentage 
of sugar varies up to from 1 to 2 per cent, in mild cases, 
and to from 5 to 10 per cent, in the severer forms. The 
total daily excretion of sugar varies up to from ten to 
twenty ounces, but it may exceed one to two pounds in the 
twenty-four hours Sugar may temporarily disappear dur¬ 
ing the course of severe intercurrent diseases. The best 
methods of detecting and estimating the sugar are by 
Fehling’s test and the fermentation-test. For details of these 
tests the reader is referred to works on urinary analysis. 

2 Excessive hunger and thirst are observed in almost all 
cases. Thirst may be a distressing symptom. As a rule, 
the food is well digested, but from the excessive amount 
taken dilatation of the stomach may occur. 

3. Emaciation is most marked in young subjects, in 


DIABETES AIELLITUS. 693 

whom the disease seems to run a more malignant course. 
The tongue is usually dry and glazed, the gums swell and 
bleed, and aphthous stomatitis may occur. Saliva is scanty. 
The skin is dry and scaly, but in some cases drenching 
sweats may occur, the perspiration being charged with 
sugar and lactic acid. Intense general pruritus is often dis¬ 
tressing, and this symptom is always highly suggestive of 
either diabetes or internal cancer. Constipation is the rule. 

4. Complicating symptoms are exceedingly numerous. 

(a) Cutaneous Symptoms. —Boils and carbuncles are com¬ 
mon, and suppurative processes are liable to follow opera¬ 
tions. Purpura is frequent. Gangrene may occur, and is 
more frequently observed in the feet. The nails may 
atrophy, and the hair may fall out. The occurrence of 
pruritus has been mentioned. 

(b) Gcnito-urinary Symptoms. —Irritation and pruritus of 
the external genitals are common. In men balanitis occurs. 
Impotence may be an early symptom. Cystitis may occur. 
The symptoms of a chronic nephritis may be added to 
those of the diabetes. 

(<:) Pulmonary complications are not uncommon. Lobar 
pneumonia, broncho-pneumonia, and gangrene of the lung 
may occur. Tubercular disease is common, and runs a 
rapid but somewhat insidious course. 

(d) Cardio-vascular Symptoms. — Symptoms of arterial 
sclerosis are commonly present, and the heart is hypertro¬ 
phied. Dilatation may ensue, and may lead to a fatal issue. 
Sudden death from fatty heart is not uncommon. 

(e) Nervous symptoms are important. 

Diabetic coma occurs especially in young subjects, and is 
usually associated with rapid emaciation. Preceding the 
onset the urine may be diminished in quantity, although the 
excretion of sugar remains unchanged. Three clinical 
forms of diabetic coma are encountered. 


694 manual of the practice of medicine. 

(1) After severe bodily or mental exertion the patient 
develops prostration with rapid and feeble heart-action, 
passes into coma, and dies within a few hours. 

(2) The patient suffers for a few days from weakness, 
constipation, dyspnoea, and abdominal pain. Then develop 
headache, restlessness, delirium, great dyspnoea amounting 
to “air-hunger,” cyanosis, and rapid and feeble heart-action. 
The breath has a sweetish odor resembling that of rotten 
apples. Coma terminates the disease within a few days. 

(3) Neither dyspnoea nor prostration appears, but the 
patient complains of sudden severe headache, feels as if in¬ 
toxicated, becomes rapidly stupid and comatose, and dies in 

a few hours. 

The exact nature of diabetic coma is unknown. It has 
been ascribed to toxaemia from acetone or from oxybutyric 
acid. In other cases it has seemed to be due to uraemia or 
to fat-embolism of the branches of the pulmonary artery 

within the lung. 

Peripheral Neuritis .—Mild forms of neuritis give rise to 
neuralgic pains, numbness and tingling, and muscular 
weakness. Severe forms cause lightning pains in the legs, 
loss of tendon-reflex, paresis of the extensors of the feet, 
and a characteristic gait. To this grouping of symptoms 
the term “ diabetic tabes” has been applied. In other cases 
paraplegia has been observed, and both hands and feet may 

be affected. 

(/) Mental symptoms consist of melancholia, and in some 

cases general paresis has resulted. 

(£■) Eye .—Cataract is common, especially in young sub¬ 
jects, and develops with great rapidity. Retinitis, hemor¬ 
rhages in the retina, optic atrophy, and sudden blindness 
have occurred. There may be paralysis of the muscles of 
accommodation. 

Prognosis.—Complete recovery cannot be expected, ah 


DIABETES MELLITUS. 695 

though a large number of patients enjoy good health for a 
number of years, and the disease in them may be controlled 
by diet. A considerable number of the cases die of heart 
failure, diabetic coma, pulmonary affections, or nephritis. 
A smaller number die exhausted and emaciated from the 
diabetes alone. As a rule, the older the patient the slower 
the course of the disease. In cases under forty years of 
age the prognosis is exceedingly grave. The cause under¬ 
lying the diabetes must always be taken into account in 
rendering the prognosis. 

The treatment is by diet and by drugs. 

Diet .—Sugars and starches should be excluded, as far as 
possible, from the food. Saccharin or glycerin may be sub¬ 
stituted for sugar. All fruits and vegetables that abound in 
starch should be prohibited; among these are potatoes, rice 
and cereals, flour- and starch-compounds, beans, peas, tur¬ 
nips, grapes, plums, apricots, pears, apples, melons, figs, 
berries, beets, onions, and asparagus. Beer, cider and 
champagne, and sweet wines should also be prohibited. 
Among other food-substances to be avoided are liver, crabs, 
lobsters and oysters, thick gravies, and soups. Theoreti¬ 
cally, bread should be prohibited, and gluten bread be given 
instead, but, as this is not readily taken by the patient, its 
use cannot in all cases be insisted upon. 

Among the articles that may be taken are butcher’s 
meat, game, poultry, fish, clams, eggs, bacon, butter, cream, 
cheese, nuts, spinach, tomatoes, cabbage, cauliflower, lettuce, 
cucumbers and pickles, gluten, bran, and almond-meal 
bread, clear soups, lemons, tea, coffee, and cocoa. 

As a rule, the diet should be modified gradually, one pro¬ 
hibited article after another being cut off. Care should be 
taken that the patient’s strength is not too far reduced by 
the restricted diet. 

Drug Treatment .—The following forms of treatment have 


6 g 6 MANUAL OF THE PRACTICE OF MEDICINE. 

been recommended, and are given in the order of preference: 
Clemens’ solution (a i per cent, solution of arsenic bromide) 
may be given in 3- to 5-drops doses after meals. Opium is 
a valuable drug, and in diabetes there exists a tolerance for 
its use. Codeia may be given in yi-g rain doses three times 
daily, and may be increased to from 6 to 8 grains in the 
day; or morphine may be given (gr. ^ doses t. i. d.), and 
increased until the daily dose is about 5 grains. The 1-grain 
opium pill may also be used. Bicarbonate and salicylate of 
sodium may be given in 1- to 2-dram doses in the day. 
Sulphide of calcium (gr. J^-ij four times a day), iodoform 
(gr. y 2 -ij four times a day), and antipyrine (gr. x-xx three 
times a day) are all occasionally of service. The alkaline 
waters of Carlsbad and Vichy may be beneficial. Jambul 
has also been employed. For the diabetic coma, venesec¬ 
tion and intravenous injections of a 3 per cent, solution of 
sodium bicarbonate have been recommended ; but recovery 
from the condition is exceedingly uncommon. 

GLYCOSURIA. 

Sugar may be found in the urine temporarily under the 
following conditions: 

1. With various forms of poisoning, such as that by 
curare, morphine, amyl nitrite, alcohol, chloroform, chloral 
hydrate, and carbon dioxide. 

2. With certain infectious diseases, especially diphtheria, 
cholera, typhoid fever, and epidemic cerebro-spinal meningitis. 

3. Gastro-intestinal disorders allowing of faulty digestion 
of sugar and starches, and with functional disturbances of the 
liver. 

4. In gouty patients with chronic diffuse nephritis. 

5. From nervous causes, as neuralgia, concussion, cerebral 
hemorrhage, etc. 

6. During pregnancy. 


DIABETES INSIPIDUS. 


69 7 


DIABETES INSIPIDUS. 

Etiology.—Diabetes insipidus is most common in young 
adults, especially in men; it not infrequently attacks 
children. Congenital cases may occur. The influence of 
heredity is frequently well marked. The disease has fol¬ 
lowed injuries and diseases of the brain and the spinal cord, 
infectious diseases, sun-stroke, sudden mental excitement, 
and the rapid drinking of large quantities of fluid. 

Pathology. —The exact nature of the disease is un¬ 
known ; it is supposed, however, to be a vaso-motor dis¬ 
turbance of the renal vessels, or, in congenital or hereditary 
cases, to be due to unnatural permeability of the blood¬ 
vessels of the Malpighian tufts. There are no essential 
post-mortem lesions. 

Symptoms.—The disease begins, insidiously or sud¬ 
denly, with the excretion of an increased quantity of urine, 
of low specific gravity. From five to ten pints daily is an 
average quantity, but from thirty to forty pints may repre¬ 
sent the daily secretion. The specific gravity of the urine 
varies from 1001 to 1004. Albuminuria and glycosuria are 
rare, although muscle-sugar, or inosite, has at times been 
found. The excretion of solids, especially of urea and the 
phosphates, may be increased in some instances. Thirst is 
inordinate, depending upon the amount of urine passed, but 
the appetite is rarely excessive. A variety of hysterical and 
neurasthenic symptoms may appear, but grave constitu¬ 
tional symptoms are usually lacking. 

Prognosis. —Spontaneous cure results in a few instances. 
In the majority of cases the disease is intractable to treat¬ 
ment, although it does not tend to shorten life. 

The diagnosis should be made from hysterical polyuria, 
the polyuria of nephritis, and diuresis from drugs. Dia¬ 
betes is to be excluded by the absence of glycosuria. 


698 MANUAL OF THE PRACTICE OF MEDICINE. 

Treatment is not very satisfactory. The most reliable 
drug seems to be valerian in full doses. Ergot has been 
recommended, but large doses are usually required. Good 
results occasionally follow the use of antipyrine in 15-grain 
doses every four hours. The bromides and arsenic have 
also been used with benefit. The constant galvanic current 
may be employed, one pole being applied to the back of 
the neck, the other pole on the lumbar region. Codeine is 
said to be of benefit, but the danger of the habit should 
preclude its use. In severe cases benefit may follow an 
exclusive diet of meat and hot water. 

SCURVY (SCORBUTUS). 

Etiology.—Devastating endemics and epidemics of 
scurvy have occurred from the earliest times among armies, 
among sailors on long cruises, and among the inhabitants 
of besieged cities, but the disease is now comparatively rare. 
Sporadic cases, however, are not infrequent, and the disease 
attacks young children more frequently than is usually 

supposed. 

Two theories as to scurvy are advanced: (1) That it is a 
dietetic disease. It is known to occur from bad and insuf¬ 
ficient food, from lack of variety in food, and from lack of 
fresh vegetables. Garrod ascribes the disease to lack ol 
potassium salts; while Ralfe believes that the disease is 
due to a diminished alkalescence of the blood, fiom diminu¬ 
tion of vegetable salts, as citrates, oxalates, and lactates, in 
the food. The development of scurvy is regularly favored 
by poor hygiene, damp dwellings, lack of sunlight, depre¬ 
ciated general health, depressing mental states, and ovei- 
exertion. The disease is equally distributed between the 
two sexes. (2) The infectious theory is that scurvy is due 
to an unknown micro-organism, and that the dietetic and 
hygienic causes are only factors predisposing to infection. 


SCUR VY. 


699 


Pathology. —The kidneys, the heart, and the liver show 
parenchymatous degeneration. The spleen is enlarged and 
soft. Hemorrhages are found beneath the skin, beneath 
the serous and mucous membranes, and in internal organs. 
Submucous hemorrhages may lead to ulcerations. 

Symptoms.—The onset of the disease is usually insid¬ 
ious, although acute cases have been described. The symp¬ 
toms are (1) general and (2) hemorrhagic. 

1. General Symptoms .—There are increasing weakness, 
pallor, and emaciation. Palpitation with feeble and irregular 
heart-action are common, and a haemic murmur usually de¬ 
velops. Mental depression and lassitude become extreme. 
The temperature is rarely elevated, and it may be subnor¬ 
mal. CEdema of the ankles may be observed. The urine 
is usually of high color and of high specific gravity, and the 
phosphates may be increased, Albuminuria is not uncom¬ 
mon. The breath is foul. The bowels are constipated. 

2. Hemorrhagic Symptoms .—The gums become spongy, 
tender, and bleed readily. These changes, however, may not 
be observed in infants and in old people. The teeth tend to 
loosen and to drop out. Ecchymoses and purpuric spots ap¬ 
pear in the extremities and spread to the trunk; they may 
arise spontaneously or after slight traumatism. Epistaxis 
is common, but hemorrhages from the lungs, the stomach, 
the intestines, and the kidneys are less frequently observed. 
Subperiosteal hemorrhages may occur, leading to pain, 
swelling, and immobility in the affected member, and ne¬ 
crosis of bone may follow, or separation of the epiphyseal 
cartilage may result in young children. Paraplegia or 
convulsions may be due to cerebral or meningeal hemor¬ 
rhage. 

Scurvy in children requires separate mention. The fre¬ 
quent occurrence of infantile scorbutus in America has been 


MANUAL OF THE PRACTICE OF MEDICINE. 


700 

brought to our notice by the able researches of Northrup of 
New York. The disease occurs in infants, usually between 
the ninth and fourteenth months, and is almost regularly due 
to an exclusive diet of proprietary food or of condensed milk. 
In rare instances it has followed the use of milk too largely 
diluted. There is no evidence that sterilized or Pasteurized 

milk can originate the disease. 

Symptoms. —The child becomes anaemic, irritable, and 
cannot bear to be handled or touched. The symptoms 
of rickets may coexist. The changes in the gums are 

almost constant, although they may not 
be carried to an extreme degree. The 
most constant symptom of infantile 
scorbutus is a painful fusiform swelling 
of the lower extremities, usually of the 
thigh. The swelling is regularly due to 
subperiosteal hemorrhages. The skin 
over the swelling is usually tense and 
shiny, is not hot to the touch, and pitting 
on pressure does not occur. The tender¬ 
ness is exquisite and is increased by 
motion. As the swelling subsides thick¬ 
ening of the shaft of the bone may be 
appreciated. Fracture of the bones and 
separation of the epiphyses may occur. 
Pseudo-paralysis is an important symp- 

Ficj. 50.—Vertical section . . c ,, • 1 

of the thigh and leg in a case tom ; it results from the pain caused 
of infantile scorbutus. The foy a contraction of the muscles pulling 

dark areas along the femur , . . . 

and tibia represent subperi- upon their tender periosteal attachment, 
osteal hemorrhage (w. p. qq iere ma y k e purpura, ecchymosis, and 

Northrup, from a specimen . 

preserved in the museum of hemorrhage from the various mucous 

Haematuria may be an 
early symptom of infantile scorbutus. 
The prognosis is good if proper diet and hygiene can be 



the College of Physicians and mem | 3 j- ane s 
Surgeons). 





RICKE TS. 


701 


enforced. Death, however, may result from weakness, from 
heart failure, or from internal hemorrhages. 

Treatment.—Sunlight, fresh air, a liberal diet of vege¬ 
tables, and orange-juice are sufficient for a cure. Orange- 
or lemon-juice is almost a specific, and in children milk and 
orange-juice practically constitute the treatment. The gums 
may be pencilled with a strong solution of nitrate of silver, 
or mouth-washes of myrrh or astringents may be used. 
Anaemia is to be controlled by iron, fresh air, and proper 
diet. The hemorrhagic symptoms are to be treated on the 
principles laid down under the consideration of purpura. 

RICKETS (RACHITIS). 

Etiology. —Rickets is a disease of the first and second 
years of life, and is rare before the sixth month, although 
cases of congenital rickets have been described. The dis¬ 
ease occurs especially in tenement-house children, from the 
combined effect of poor air, scanty sunlight, and defective 
food. The most common of the dietetic errors that may 
lead to the disease are premature weaning, the use of arti¬ 
ficial and proprietary foods, especially those composed 
mainly of farinaceous and starchy ingredients, irregular 
feeding, prolonged lactation, and nursing during pregnancy. 
Children of weak or vicious parentage seem to be predis¬ 
posed to the rachitic condition. The disease is more com¬ 
mon among negroes and in European cities than among 
American children. The connection between syphilis and 
rickets has not been proven satisfactorily. Rickets is often 
delayed until the third or fourth year, and then may appear 
as a sequel to some infectious disease such as measles. 
The disease known as “ acute rickets ” is now supposed 
to be scorbutus. 

Pathology. —The lesions are seen in their fullest develop¬ 
ment in the long bones and in the ribs. The epiphyseal 


702 MANUAL OF THE PRACTICE OF MEDICINE. 

cartilages undergo rapid proliferation, and form thick, soft 
cushions, which by their projection may present evident 
bulging. The periosteum strips readily, and subperiosteal 
tissue is seen to be soft and vascular, lesembling spleen- 
pulp. This subperiosteal thickening is best marked in the 
middle of the shaft of the bones, giving to them a spindle 
shape. There is regularly delay or arrest of ossification- 
processes, and in the bones the organic ingredients may be 
reduced to two-thirds of their normal proportions. Rachitic 
bones are regularly soft, spongy, and vascular, especially 
near the epiphyses and beneath the periosteum. From the 
bone-softening various deformities arise the box-like 
cranium, spinal curvature, deformed pelvis, knock-knee, 
bow-legs, and the like. In time there occur in the carti¬ 
lages and in the subperiosteal tissues reconsti uctive changes 
resembling the callus-growth upon fractures, and the bones 
themselves become hard. In this way permanent deformi¬ 
ties result. The liver and the spleen are usually enlarged 
in rickets. 

Symptoms. —Certain prodromal symptoms may precede 
evident changes in the bones. Gastro-intestinal disorders 
are usually present, and a peculiar form of diarrhoea limited 
to the first part of the day, with scanty colorless stools, has 
been described. There may be attacks of screaming at 
night, and restlessness with an intermittent temperature and 
splenic enlargement. Profuse night-sweats about the neck 
and the back of the head are highly suggestive of incipient 
rickets. There is often such extreme soreness of the body 
that the child cries when handled. This diffused soreness 
is a most suggestive symptom. The child becomes flabby 
and anaemic, and usually emaciates. There may be “ pseudo¬ 
paresis,” from a combination of muscular weakness and dis¬ 
inclination to move on account of the general soreness and 
tenderness. 


RICKETS . 


7°3 


Nervous symptoms often are present. Attacks of spasm 
of the larynx are not uncommon. Convulsions, either 
general or partial, may appear at intervals; the convulsions 
may be fatal. Tetany and carpopedal spasms may be 
observed. The child is irritable and nervous. 

Symptoms due to changes in the bones are seen first in the 
ankles, wrists, ribs, and cranium. The epiphyseal ends of 
the bones are swollen; the bones are liable to curvature, 
and “ green-stick ” fractures may be caused by slight injuries. 
Curvature of the spine (rachitic scoliosis and kyphosis) and 
pelvic deformities may ultimately result. The thorax shows 
noticeable changes. The swellings at the junction of the 
ribs with their cartilages produce visible nodules, to which 
the name “ rachitic rosary ” has been applied. The lateral 
portions of the thorax are frequently drawn inward at the 
portions corresponding with the insertion of the diaphragm. 
“ Pigeon-breast ” may occur. The changes in the thorax 
may be so marked as to interfere with proper chest-expan¬ 
sion, so that pulmonary affections trifling to the non-ra- 
chitic may become serious diseases in these children. The 
clavicles may be distorted or fractured. 

Characteristic changes become apparent in the cranium. 
The fontanelles remain unclosed until the second or third 
year of life, and the occiput may be so thin and yielding 
that it can be pressed in like parchment. To this latter 
condition the name “ craniotabes ” has been applied. The 
head becomes large and square. The occiput is flattened, 
the biparietal diameter is increased, the frontal bones are 
broad and prominent. The square, box-like cranium may 
resemble hydrocephalus, but in rickets the child is men¬ 
tally bright. 

The maxillary bones are small and narrowed, and the 
vaulting of the roof of the mouth is increased. Dentition 
is late, and the teeth may be ill formed, small, or irregularly 


704 MANUAL OF THE PRACTICE OF MEDICINE. 

crowded. Prom the diminished growth of the bones the 

child may be stunted and dwarfed. 

The prognosis is good for the disease itself, but many 
rachitic children fall victims to gastro-intestinal or pulmon¬ 
ary disorders. The prognosis should also regard the ulti¬ 
mate effect of the thoracic spinal and pelvic defoimities. 

Treatment.—The most important treatment is improve¬ 
ment of the general condition by proper diet, good air, sun¬ 
shine, and salt-water baths. Anaemia is to be treated by 
syrup of the iodide of iron, and digestive disturbances 
should receive prompt attention. The child should lie on 
a hair mattress or pillow, and should not be allowed to walk 
so long as the bones are soft. Theoretically, preparations 
of lime, such as the calcium lactophosphate, are indicated, 
but as a matter of experience they do very little good. The 
drug par excellence is phosphorus, which should be given 
in doses of gr. three times a day in cod-liver oil. The 
deformities ultimately require special gymnastic exercises 
for their correction, or orthopaedic treatment. 

PURPURIC DISEASES. 

Under this heading are included a number of diseases 
having one symptom in common—the extravasation of 
blood under the skin. Small hemorrhagic spots are known 
as “ petechiae larger hemorrhages are called “ echymoses.” 
Various degrees of intensity are met with in each variety of 
purpuric disease. The mildest form consists of subcuta¬ 
neous hemorrhages alone; the severer forms include as well 
hemorrhages from free mucous surfaces and visceral hemor¬ 
rhages. Thus purpura may be a trifling, a senous, or even 
a fatal disease. The following classification may be adopted, 
although it should be remembered that transitional forms are 
frequently encountered: I. Symptomatic purpura; 2. Pur¬ 
pura rheumatica; 3. Purpura hsemorrhagica. 



PURPURIC DISEASES. 


7 05 


Symptomatic Purpura. 

1. Toxic cases following certain drugs, such as potassium 
iodide, chloral hydrate, quinine, copaiba, and more rarely 
ergot, mercury, and belladonna. 

2. Severe infectious diseases, such as acute yellow atro¬ 
phy of the liver, snake-bites, typhoid fever, pneumonia, 
and the exanthemata. 

3. Severe continued jaundice. 

4. Profound ancemia, leukaemia, pseudodeukcemia, scurvy, 
and exhausted and cachectic conditions. 

5. New-born children with congenital syphilitic change in 
the arterial walls. 

6. New-born children without arterial change. This form 
occurs in I per cent, of children, with a mortality of 75 per 
cent. 

7. Embolic cases with malignant endocarditis and with 
multiple sarcoma. 

8. Neurotic cases, from vaso-motor relaxation or enfeeble- 
ment of the arterial walls, after fright, deep emotion, 
hysteria, hypnotism, severe neuralgias, and inflammations 
of the spinal cord. 

Symptoms. —Secondary purpura may occur with sub¬ 
cutaneous hemorrhages alone, or with free and visceral 
hemorrhages as well. Arthritic pains may occur as in 
purpura rheumatica. 

Purpura Rheumatica (Peliosis Rheumatica, or 
Schonlein’s Disease). 

This affection is most common between the ages of 
twenty and thirty, and is more frequent in males than in 
females. An antecedent history of rheumatic fever is fre¬ 
quently obtained, but the exact relationship of the disease 
to rheumatism has not been determined satisfactorily. 

Symptoms. —The disease usually begins with a sore 
45 


70 6 MANUAL OF THE PRACTICE OF MEDICINE. 

throat, malaise, moderate fever, and pain in the joints. The 
gums are not affected as in scurvy. The articular pain and 
swelling are due to small hemorrhages in and about the 
joints. More rarely arthritis with serous or hemorrhagic 
effusion occurs. Purpura precedes or accompanies the 
articular pains, and there are frequently associated urticarial 
wheals which may be hemorrhagic, or any of the manifesta¬ 
tions of erythema. Hemorrhagic pemphigus may also occur. 
The urine may contain albumin. 

The duration of the disease is between ten days and 
three weeks. Relapses are common, especially if the patient 
walk too soon. 

The prognosis is perfectly good. 

Purpura Hemorrhagica (Morbus Maculosus, or 
Werlhoff’s Disease). 

Under this heading are included cases of purpura having 
a disposition to bleed from the mucous membranes and 
into internal viscera. Severe cases of secondary purpura 
may be thus included. In some cases purpura haemor- 
rhagica runs a course more like that of an infectious 
disease. An acute and a subacute form may be described. 

Acute Purpura Hemorrhagica (Fulminating Purpura). 
—The acute form is more common in young adults, but is 
a rare condition. 

1. In some cases the patient is seized with a chill, fever 
rising to 103° or 104° F., and intense prostration. Purpuric 
spots rapidly appear, and bleeding occurs from any of the 
mucous membranes. The patient passes into stupor alter¬ 
nating with restlessness and mild delirum, and dies, either 
from the hemorrhages or in coma, in from one to seven 
days. The prognosis is bad, 75 per cent, of all cases ter¬ 
minating fatally. 

2. In other cases the visceral hemorrhages are the excit- 


PURPURIC DISEASES. 


707 


ing cause of death. Cerebral and meningeal hemorrhages 
are usually multiple and show no favorite seats of selection. 
Hemorrhage into the suprarenal capsules may cause death 
in collapse within a few hours. 

3. When the disease attacks pregnant women, miscar¬ 
riage and severe post-partum hemorrhage result, and the 
disease runs a rapid, and usually a fatal, course. 

Symptoms.— Subacute Purpura Hyemorrhagjca.— 
Prodromal symptoms may precede the actual onset; these 
symptoms comprise malaise, chilly feelings, and a slight 
evening rise in temperature. 

Constitutional Symptoms .—An initial chill may occur, but 
usually chilly feelings are scattered throughout the course 
of the disease. The temperature varies from ioo° to 104° F., 
and is higher in severe cases and in children. Prostration 
is a marked and constant symptom, and usually persists 
during convalescence. In severe cases the “ typhoid con¬ 
dition ” may be developed, and in this condition the patient 
may die. The spleen and the liver are usually enlarged 
during the attack, and a light form of jaundice is not un¬ 
common. The blood rapidly shows the changes of anaemia. 

Hemorrhagic Symptoms .—Purpura develops, the hemor¬ 
rhagic areas varying from pin-head size to that of the palm 
of the hand. Extensive ecchymoses may be followed by 
gangrene of the skin. Free hemorrhages occur from any 
of the mucous membranes, the most frequent sources of 
bleeding being respectively the nose, the kidney, the intes¬ 
tines, and the uterus. These hemorrhages may be moder¬ 
ate, or they may be so profuse as to induce a fatal anaemia. 
Internal hemorrhages into the brain and its membranes, the 
lungs, or the adrenals may occur, but they are not as com¬ 
mon as in the acute form. Pain and swelling of the joints, 
especially of the hands, the feet, and the knees, may be ob¬ 
served. The articular symptoms are identical with those 


708 manual of the practice of medicine . 

seen in peliosis rheumatica. In rare cases ankylosis or 
arthritis may develop. The gums may be normal, or they 
may be swollen and may bleed, but the teeth are not loos¬ 
ened as in scurvy. 

The pathology of the disease is unknown. Letzerich 
has described a bacillus which grows in the liver and enters 
the blood-vessels, causing in the smaller vessels hyaline 
thrombi which so weaken the internal wall as to allow of 
hemorrhage; but his experiments have not been sufficiently 
verified. 

The duration of the disease varies from several days to 
several weeks, but by relapses the disease may be protracted 
for months or even for years. 

The prognosis is usually good, but death may result 
from anaemia, from fatty degeneration of the heart, from 
exhaustion, or from visceral hemorrhages. 

Henoch's Disease .—A severe form of subacute purpura 
haemorrhagica has been described by Henoch and bears his 
name. This form occurs especially in children between the 
ninth and twelfth years, although it has occurred between 
the ages of three and forty-six. Males are affected five 
times as frequently as females. There is a prodromal period 
with malaise, slight fever, and pain in the joints. The onset 
is characterized by purpura, pain and swelling of the joints, 
and severe gastro-intestinal symptoms. These latter symp¬ 
toms consist of abdominal tenderness with a colicky pain 
of great severity. The abdomen is rigid and retracted. 
Rectal tenesmus occurs, with bloody stools. Vomiting is 
severe, and the vomited matters may contain blood. These 
gastro-intestinal symptoms seem to be due to hemorrhages 
in the submucosa or to hemorrhagic infarcts of the small 
blood-vessels of the intestinal wall. Intestinal ulceration, 
perforation, and peritonitis may result. The spleen is 
enlarged. The temperature is slightly raised. Haematuria 


haemophilia. 


709 

occurs in one-fifth of the cases. These symptoms continue 
for a few days and then subside, but relapses are the rule ? 
and as many as twenty subsequent attacks have been de¬ 
scribed. The nature of the disease is unknown. 

Ihe prognosis is fairly good, being better in children 
(5 per cent, mortality) than in adults, of whom 25 per cent, 
die. 

Treatment of Purpuric Diseases. 

In the secondary purpuras the treatment should be 
directed toward the exciting causes. In the other forms the 
treatment is supporting and symptomatic. Arsenic in full 
doses is at times of service. Iron is indicated for anaemic 
conditions, but it should be withheld during the acute 
attacks, as it seems to increase the liability to hemorrhage. 
In all cases fresh air, good food, and a tonic supporting 
treatment are indicated. The salicylates are at times of 
service in peliosis rheumatica, but in some cases they seem 
useless. 

For the hemorrhages various drugs may be used, but no 
one hemostatic can be relied upon. Among the drugs used 
are aromatic sulphuric acid, turpentine, acetate of lead, and 
gallic acid. Epistaxis may require plugging of the nares. 

Menorrhagia may be controlled by firm tamponage. 

In acute purpura free stimulation is necessary, and in 
case of profuse hemorrhage rectal or hypodermic injections 
of sterilized saline solutions should be employed. 

In subacute purpura much benefit may be derived from a 
change of climate, inland places where the air is dry and 
bracing being preferable. 

HAEMOPHILIA. 

Etiology.—By “ haemophilia ” is meant a constitutional 
inherited tendency to uncontrollable bleeding. The disease 
appears in males in the proportion of 13 : 1. Females rarely 


710 MANUAL OF THE PRACTICE OF MEDICINE. 


suffer, although the female members of a bleeding family 
transmit the tendency to their male offspring. Paternal 
transmission is exceedingly rare. In rare instances the 
tendency is acquired. 

Pathology.—The exact nature of the disease is unknown. 
An unusual thinness of the arterial walls has been observed, 
but this condition is inconstant. The joints may be found 
to be the seat of hemorrhages, and inflammation of the syno¬ 
vial capsule has been described in a few instances. 

The symptoms generally appear in early childhood, al¬ 
though excessive bleeding does not usually accompany the 
cutting of the umbilical cord. The symptoms consist of 
hemorrhages and inflammation of the joints. The hemor¬ 
rhages may be spontaneous or may follow traumatism. 
Cuts or abrasions bleed profusely, and continuous capillary 
oozing may continue for days after the extraction of teeth. 
Epistaxis is commonly profuse. These hemorrhages weaken 
the patient and may at any time prove fatal. Subcutaneous 
hemorrhages evince themselves as purpuric spots, ecchy- 
moses, and haematomata. Large ecchymoses may be suc¬ 
ceeded by gangrene. In the female menstruation may be 
profuse, but parturition is rarely complicated by hemor¬ 
rhage. The joint-symptoms usually occur after exposure 
to cold, to which haemophilic patients are exceedingly sus¬ 
ceptible. Pain and swelling occur, especially in the larger 
joints, and the condition may closely resemble rheumatism. 

Prognosis.—Haemophilia is a contant menace to life. 
Half the cases die before the seventh year, and only one- 
eighth reach majority. The younger the patient the more 
serious the prognosis. The prognosis is better in girls 
than in boys. Although a serious condition, haemophilia 
is not inconsistent, in some instances, with a prolonged and 
busy life. 

Treatment.—Sons born to female members of bleeding 

o 


HAL MO PHIL I A . 


7 ii 

families should be protected from external injuries, and the 
system should be fortified by fresh air and general hygiene. 
Surgical operations, however slight, should be resorted to 
only when absolutely indicated, and every appliance should 
be at hand to check hemorrhage. The hemorrhages, when 
they occur, should be treated by compression and by the 
application of the well-known haemostatic remedies. For 
the joint-affections rest and soothing applications are in¬ 
dicated. 


VII. DISEASES OF THE BLOOD AND THE 
LYMPHATIC GLANDS. 


ANAEMIA. 

Anemia is a generic name applied to deficiencies in the 
quality or quantity of the blood or of its important constitu¬ 
ents. The quantity of the blood may be diminished (oligae- 
mia), or the number of the red corpuscles may alone be 
diminished (oligocythaemia). In other cases such important 
constituents as albumin or haemoglobin may suffer diminu¬ 
tion (oligochromaemia). The following classification of 
anaemia is generally adopted: i. Secondary anaemia; 2. 
Chlorosis ; 3. Pernicious anaemia. 

Secondary Anjemia. 

Etiology.—The causes of secondary anaemia have been 
conveniently classified by Osier as follows : 

1. Ancemiafrom hemorrhage. 

2. Long-continued drain on the albuminous materials of the 
blood, as in chronic suppuration, Bright’s disease, prolonged 
lactation, or rapid-growing tumors, as cancer. 

3. Ancemia from inanition and defective nutrition , as from 
insufficient or improper food, digestive disturbances causing 
malassimilation, improper modes of life, and intestinal 
parasites. 

4. Toxic ancemia results from the use of certain drugs, as 
lead, mercury, arsenic, salicylic acid, or from organic poison¬ 
ing, as in syphilis, malaria, infectious diseases, tuberculosis, 
and pyrexia. 

712 



ANAEMIA. 


71 3 


Pathology.—In secondary anaemia the number of the 
red corpuscles and the percentage of haemoglobin are pro¬ 
portionately diminished. In severe forms some of the cells 
may be unnaturally small (microcytes) or of irregular sizes 
(poikilocytes). Nucleated red cells are always found, al¬ 
though their number may be small in the mildest grades 
of anaemia. In anaemia after hemorrhage a primary in¬ 
crease in the number of the white corpuscles is usually 
noticed. The restoration of the watery, saline, and albu¬ 
minous materials rapidly occurs by absorption, but the 
regeneration of the red cells is a slower process. Restora¬ 
tion of the normal percentage of haemoglobin is the last 
process of regeneration. 

General Symptomatology of Anaemia.— 1. Pallor of the 
skin and the mucous membranes. It must be remembered 
that not all anaemic patients are pale, and that not all pale 
patients are anaemic. Anaemic pallor is best appreciated 
by the colorless appearance of the ears. In suspected cases 
of anaemia more reliance should be placed upon the results 
obtained by counting the red blood-cells and estimating the 
percentage of haemoglobin than upon the appearance of 
the patient. 

2. Cardiac Symptoms .—The pulse is rapid and usually 
of low tension. Occasionally a high-tension pulse is en¬ 
countered. The heart-action is irritable. Palpitation and 
syncopal attacks are common. In acute anaemia death from 
syncope may occur. The heart, being supplied with blood 
of poor quality, tends to become fatty and loses its muscular 
tone. Mild grades of dilatation are common. A systolic 
haemic murmur may be heard over the pulmonary area and 
is transmitted upward. This murmur comes and goes, and 
is often appreciated only while the patient lies down. The 
origin of the anaemic murmur is obscure. There may be 
heard at the apex a systolic murmur transmitted to the 


714 MANUAL OF THE PRACTICE OF MEDICINE. 

axilla. This murmur arises from relative mitral insufficiency 
occasioned by poor muscular contraction, or from slight 
dilatation of the left ventricle. A continuous venous hum 
(the bruit de diable) may be heard over the jugular vein on 
the right side of the neck. In extreme anaemia there is a 
tendency to thrombus-formation, especially in the femoral 
vein. Unless thrombus occur in the cerebral sinuses, the 
condition is not serious. 

3. Dyspeptic symptoms are rarely absent. The tongue is 
flabby and coated. The bowels are constipated; the appe¬ 
tite is irregular and capricious. 

4. Pulmonary Symptoms .—Dyspnoea on exertion is in 
proportion to the extent of the anaemia and the rapidity 
of its development. In acute anaemia from hemorrhage 
there may be “ air-hunger.” A slight cough without expec¬ 
toration not infrequently occurs. 

5. Cerebral Symptoms .—There is regularly mental apathy 
and loss of the power of concentrating the mind. Spots be¬ 
fore the eyes, buzzing noises in the ears, and vertigo indicate 
cerebral anaemia, whether of general or local origin. Head¬ 
aches, usually more marked in the top of the head and 
increased by standing, are frequent, but other forms of 
headache due to digestive disturbances are commonly en¬ 
countered. 

6. There are body-weakness and lack of endurance. The 
inability to exercise is often aggravated by the dyspnoea 
thus induced. Slightcedema of the ankles or the legs is not 
uncommon. An irregular low temperature may be noted 
in severe cases. Emaciation does not belong to simple 
anaemia. If present, some primal cause, as tuberculosis or 
cancer, should be suspected. 

7. Menstruation is often affected. There may be menor¬ 
rhagia, but, as a rule, the menses become scanty and light- 
colored or may even cease. Amenorrhoea is of no signifi- 


ANAEMIA. 


7 15 


cance and demands no special treatment, as it is nature’s 
method of preventing further drains upon the already im¬ 
poverished blood. 

8. Nervous and hysterical symptoms are usually present. 
The patient becomes irritable and restless, sleepless by 
night, drowsy by day, and may complain of various nervous 
symptoms, such as hot and cold flashes, irregular pains, and 
curious sensations in the skin. 

The diagnosis of anaemia is rendered positive by the 
results of blood-examination. For methods of counting 
the corpuscles and of calculating the percentage of haemo¬ 
globin the reader is referred to books on clinical diagnosis. 
The diagnosis should never rest with the detection of 
anaemia, but must extend to the discovery of the cause, to 
which the blood-condition is secondary. 

Treatment.—The primal cause, if possible, should be re¬ 
moved by correcting improper modes of life and controlling 
digestive errors and constipation. The value of fresh air 
and sunlight cannot be over-estimated, but it is equally im¬ 
portant not to over-fatigue anaemic patients by keeping them 
walking or exercising all day, as is sometimes done. 

The specific drug for anaemia is iron. The special prep¬ 
aration used should not be such as to cause constipation 
or headache. The preparations recommended are Blaud’s 
pill (gr. v, t. i. d.), tartrate of iron and potassium in 10-grain 
doses in water and glycerin (Price’s English glycerin should 
be used), citrate of iron and quinine, the pyrophosphate of 
iron, and the liquor ferro-mangans of Gude or of Dietrich. 
During the administration of iron the bowels must be moved 
daily, preferably by salines given in the morning. Should 
iron not be well borne, arsenic or small doses of bichloride 
of mercury or of binoxide of manganese may be given. 
In severe cases rest in bed at the beginning of the treat¬ 
ment is to be recommended. 


716 MANUAL OF THE PRACTICE OF MEDICINE. 


Chlorosis. 

Etiology and Symptoms.— This condition is common to 
women between the ages of fourteen and twenty-four. 
More rarely the affection is encountered in males at the age 
of puberty. Blondes are more frequently attacked than bru¬ 
nettes. The disease is especially frequent in over-worked 
factory-girls who live amid poor hygienic surroundings and 
who work hard upon insufficient or improper food; but 
cases among the upper classes are not uncommon. Young 
female immigrants are often attacked soon after their arrival 
in America. There seems to be some connection between 
chlorosis and puberty, as in many cases there is the history 
of precocious development and the early appearance of the 
menses; in other cases the menses may be retarded. Sir 
Andrew Clark attributed chlorosis to a blood-poisoning 
from the absorption of toxic products from a constipated 
bowel. In some cases it would seem that chlorosis had a 
primary nervous origin. Mothers chlorotic in their youth 
are apt to beget chlorotic daughters. In a few instances 
chlorosis seems to be due to a congenital lack of develop¬ 
ment of the arterial system (Virchow). Synonyms: Chloro- 
anaemia; Green sickness. 

Pathology. —The essential blood-change consists in the 
reduction of haemoglobin. In average cases the haemoglobin 
falls to 40 per cent., in severe cases to 20 per cent. The 
number of the red cells may be normal, although, as a rule, 
they are considerably reduced, but never to the same pro¬ 
portional extent as the haemoglobin. In a series of 63 
cases reported by Osier the average reduction in the num¬ 
ber of red cells was 74 per cent.; the average quantity of 
the haemoglobin was 42.3 per cent. Poikilocytes, micro¬ 
cytes, and a small number of nucleated red blood-cells may 
be seen. 


ANAEMIA. 


717 


Symptoms. —Anaemic symptoms arc constant, especially 
those of nervous and dyspeptic origin. Amenorrhcea is 
most commonly observed. The color of the skin is not 
that of anaemia, but is a pale greenish-yellow that is quite 
characteristic. 

There has been described a gastric type of chlorosis with 
nausea, vomiting, and epigastric pain as prominent symptoms. 
There may even be vomiting of blood, so that the case may 
resemble one of gastric ulcer. The diagnosis in these cases 
from gastric ulcer is often one of great difficulty, and is 
rendered more uncertain by the fact that gastric ulcer not 
uncommonly occurs in chlorotic women. 

The appetite is apt to be capricious and is even perverted. 
Constipation is usually constant and obstinate. Emaciation 
does not occur. CEdema of the ankles may be noticed, 
and there may be an irregular fever. The cardiac symp¬ 
toms of anaemia are usually well marked. 

The prognosis is good for recovery, but relapses are 
common, and by them the course of the disease may be 
prolonged. Relapses may occur even during the third 
decade of life. 

Treatment is usually followed by brilliant results if the 
patient faithfully carries out the directions. Iron is a 
specific, and under its use the haemoglobin increases from 5 
to 10 per cent, each week. The patient rapidly improves 
under its use, and often feels capable of discontinuing the 
treatment, but it is important to continue treatment until the 
haemoglobin is above 90 per cent., as otherwise the patent 
is apt to relapse. The cure in average cases is obtained by 
about three months’ treatment. 

Fresh air, good nourishing food, improved hygiene, and 
the daily use of laxatives, if needed, are important adjuvants 
to the medicinal treatment. In severe cases a short rest in 
bed at the beginning of the treatment is often of incalcula- 


yi 8 MANUAL OF THE PRACTICE OF MEDICINE. 

ble service. In the chlorosis of young immigrants per¬ 
oxide of manganese or permanganate of potassium in 2- 
grain doses three times a day may be advantageously com¬ 
bined with the iron. 

Pernicious Anemia. 

Synonyms. —Essential anaemia ) Idiopathic anaemia. 

Under the heading 14 pernicious anaemia are included 
cases of anaemia running a progressive course and not due 
to any evident cause. Severe secondary anaemia, resem¬ 
bling the pernicious form in its clinical features, may follow 
atrophy of the stomach and certain intestinal parasites, 
especially the bothriocephalus latus and the ankylostoma 
duodenale, but it is doubtful whether these secondary cases 
are to be considered as examples of the true pernicious 
anaemia. 

Etiology. —The disease is one of adult life; more rarely 
it attacks children. Both sexes are equally affected. In 
some cases there is a history of pregnancy or of parturition; 
in other cases no assignable cause for the anaemia can be 
found. 

Pathology.— The essential lesions are found in the blood, 

the liver, and the bone-marrow. 

The blood is diminished in quantity and is pale and 
watery. The number of the red blood-corpuscles is greatly 
reduced, in some instances to as low as one-tenth or less of 
their normal number (500,000 to the cubic millimeter is not 
an uncommon reduction ; in one instance the number was 
reduced from the normal 5,000,000 to 143,000). The per¬ 
centage of haemoglobin may be reduced in proportion to 
the reduction in the number of the red cells, or it may even 
be relatively increased. It is pathognomonic of pernicious 
anaemia that each red corpuscle remaining in the blood 
carries its normal, or even more than its normal, load of 


ANAEMIA. 


719 


haemoglobin. Large and small red corpuscles are seen in 
the freshly drawn blood (“ megalocytes ” and “ micro¬ 
cytes ”), and the corpuscles may be deformed, flask-shaped, 
and distorted (“ poikilocytes ”). Nucleated red cells are 
constantly present, and, if present in large numbers, are dis¬ 
tinctive only of pernicious anaemia and of the last stages of 
leukaemia. In dried and stained specimens of blood two 
varieties of nucleated cells are seen—one normal in size, 
with a sharply defined nucleus (“ normoblast ”), and others 
of large size, with large, poorly-stained nuclei (“ giganto- 
blasts ”). The leucocytes are generally diminished in 
number. 

The liver may be enlarged and fatty. The peripheral 
zones of the acini are pigmented by iron—a condition, in all 
probability, characteristic of pernicious anaemia. 

The bone-marrow shows an increase of lymphoid and nu¬ 
cleated red cells, and resembles the red marrow of the child. 

There is found fatty degeneration of the heart, the 
kidneys, and the intima of the smaller blood-vessels. The 
spleen may be normal or slightly enlarged, and may be 
pigmented by iron. The lymphatic glands may resemble 
spleen-pulp in consistency and color. Hemorrhages are 
usually found under the skin and the mucous and serous 
membranes. 

Two theories of pernicious anaemia have been advanced: 

1. Hunter maintains that, by reason of faulty gastro¬ 
intestinal digestion, toxic products gain access to the liver 
and cause extensive blood-destruction, with the deposit of 
pigment in the liver and the passage of urobilin by the 
kidneys. Hunter’s views, although not absolutely proven, 
are those generally adopted. 

2. The second theory is that there is an increased ten¬ 
derness or vunerability of the blood-corpuscles, from faulty 
processes in blood-manufacture. 


720 MANUAL OF THE PRACTICE OF MF.D1C1NE. 

The symptoms are those of progressive anaemia. The 
color of the patient is a peculiar waxy white or pale lemon. 
The fat is usually well preserved, and the patient presents a 
bloated appearance. Syncopal attacks are frequent, and fatal 
syncope, from fatty degeneration of the heart, may occur. 
In some cases capillary pulsation and visible pulsation of the 
arteries may be as well marked as in aortic regurgitation. 
Haemic murmurs and slight dilatation of the left ventricle 
are almost constant. An irregular temperature develops 
from time to time—usually ioo° or ioi F., more raiely 
from 102° to 104 0 F. At other times the temperature may 
be subnormal. 

The urine is suggestive of the disease; it is of low 
specific gravity and of high color, and it contains an excess 
of urobilin. The pigmentation of the mine, however, is 
not constant. Gastro-intestinal symptoms of anaemia aie 
common; diarrhoea, however, may not be infrequent. 
Dropsical swelling of the ankles attends the later stages 
of the disease, and the dropsy may become general. The 
tendency to hemorrhage is seen in purpuric spots and in 
submucous ecchymoses. Retinal hemorrhage is not uncom¬ 
mon. Free hemorrhages from mucous surfaces, with the 
exception of epistaxis, are rather infrequent. 

Prognosis. —The course of the disease is progressive, 
with periods of temporary improvement, but cases of 
apparent recovery are not uncommon since the inaugura¬ 
tion of the arsenic treatment. Death is usually preceded 
by a prolonged state of prostration, stupor, and mild 

delirium with irregular fever. 

Diagnosis.— According to Osier, the following are the 
essential points : (i) The severe grade of reduction in the 
number of the red cells; (2) their relative richness in 
haemoglobin; (3) the presence of many megalocytes and 
gigantoblasts ; (4) the absence of any cause for secondary 


ANAL MIA. 


721 


anaemia; (5) occasional febrile disturbances; (6) the yellow 
tint of the skin; (7) hemorrhages, particularly retinal; (8) 
a progressive course and the inefficiency of treatment. 

Treatment.—Iron in pernicious anaemia seems to be 
worthless. The main reliance must be placed on arsenic 
in full doses, given to the point of tolerance. Osier’s plan 
is to give Fowlers solution in 3 -m, nim doses after meals, 
increased to 5 minims at the end of the first week, to 10 
minims at the end of the second week, and so on until the 
patient is taking 20 or 25 minims after each meal. Toxic 
symptoms are rare. Should they occur, the drug is to be 
discontinued until the poisoning symptoms cease, and is 
then to be resumed at the dose at which the patient left 
off In some cases the addition of phosphorus seems to 
be beneficial. Iron may be given if arsenic disagrees, but 
not much is to be expected from it. Rest in bed from time 
to time is important in conserving the patient’s strength. 
Prolonged residence in a warm inland climate has been 
recommended, but the climatic treatment is often disap¬ 
pointing. The diet should be light and nutritious. Mas¬ 
sage is sometimes found to be beneficial. 

Delafield describes a clinical set of cases midway between 
simple and pernicious anaemia, occurring in those past 
middle life. The etiology of these cases is obscure. The 
blood shows the changes only of secondary anaemia. The 
symptoms are those of a fairly marked anaemia, but im¬ 
provement under treatment reaches only to a certain degree, 
and the patients relapse as soon as treatment is discon¬ 
tinued. Absolute recovery does not occur. In this class 
of cases arsenic seems to be of no use. Iron is the druo- 
on which reliance is to be placed, but dietetic and hygienic 
treatment seems to be of almost equal service. 


46 


722 MANUAL OF THE PRACTICE OF MEDICINE. 

LEUCOCYTOSIS. 

By the term “ leucocytosis ” is meant a temporary increase 
in the number of the white blood-corpuscles ; this is a con¬ 
dition entirely distinct from the disease leukaemia. Nor¬ 
mally the ratio of white to red corpuscles is I : 500, but in 
leucocytosis the proportion may be 1 : 150 or even 1 : 50. 

Physiological leucocytosis occurs during pregnancy and 
after hearty eating. 

Inflammatory leucocytosis occurs in acute infectious dis¬ 
eases attended with local inflammatory reaction. It appears 
most commonly with pneumonia, diphtheria, and suppura¬ 
tive processes, and it is said to be a sign of good prognostic 
value. 

Cachectic leucocytosis occurs in the cachexias of malignant 
tumors. 

Relative leucocytosis occurs in anaemia, where, from 
diminution in the number of the red corpuscles, the white 
cells appear in an increased ratio, although they are not 
actually increased in number. 

LEUKAEMIA (LEUCOCYTELEMIA). 

Etiology— The cause of the disease is obscure. There 
occur acute cases which suggest bacterial infection, but 
upon this point definite knowledge is lacking. In about 
one-third of the cases there is the history of malarial poison¬ 
ing. Syphilis seems to possess some obscure relation to 
the disease. Leukaemia may occur at any age, but it is 
most common in middle life. Males are affected twice as 
frequently as females. In women the disease often appears 
at the time of the climacteric or after pregnancy. 

Pathology. —The essential lesions are found in the blood, 
the spleen, the lymphatic glands, and the bone-marrow. 
The blood-changes are constant. According to the relative 


LEUKAEMIA. 


723 


intensity of the changes in the other structures mentioned, 
splenic (or lienteric), lymphatic, and myelogenous forms have 
been described. As true myelogenous leukaemia is so very 
rare, the disease is usually described under two principal 
forms, (1) splenic-myelogenous or lieno-myelogenous, and 
(2) lymphatic leukaemia. 

Blood-changes consist in the increased number of white 
cells, their proportion to the red corpuscles rising to 1 : 20 
or 1 : 5, or the cells even being in equal proportions. The 
increased proportion is greater in the splenic-myelogenous 
form than in lymphatic leukaemia. The blood is pale and 
watery and may be whitish or brownish-red in color. The 
red cells are diminished, but not to an excessive degree; 
haemoglobin is reduced to a somewhat greater proportion. 
Nucleated red cells may be seen. Charcot’s octahedral 
crystals separate when blood-slides are kept for some time. 

A more detailed account of the changes of the white cells is deemed 
advisable. 

In the normal blood, Ehrlich describes the following varieties of white cells : 

1. Lymphocytes, small, equal in size to a red corpuscle. The nucleus is large, 
round, stains deeply, and is surrounded by a narrow rim of non-granular 
protoplasm. 

2. Large 7 nononuclear leucocytes, several times larger than the red cells. 

I he nucleus is oval or elliptical and is surrounded by a wide margin of non- 
granular protoplasm. 

3. A transition form resembling the preceding, but the nucleus is inden- 
tated. 

4. Polynuclear leucocytes, smaller than the large mononuclear forms, with 
^ on &j twisted nuclei which stain deeply. The protoplasm is granular and 
does not stain easily. To these cells, owing to peculiarities of staining, the 
name “ neutrophiles ” is given. 

5. Cells like the preceding, but the protoplasm contains coarse granules 
which stain deeply with eosin, hence the name “ eosinophiles.” 

In normal blood these varieties of white cells bear a fixed proportion to 
each other—the lymphocytes, from 15 to 30 per cent., the polynuclear leuco¬ 
cytes, from 65 to 80 per cent., the mononuclear and transitional forms, 6 per 
cent., the eosinophiles, from 2 to 4 per cent. According to Osier, the charac- 


724 MANUAL OF THE PRACTICE OF MEDICINE. 


ter of the cells in splenic-myelogenous leukaemia differs materially from that 
in the lymphatic form. 

In splenic-myelogetious leukamia the lymphocytes are rarely, if at all, in¬ 
creased ; the eosinophiles are present in normal or increased proportion, so 
that there is a great total increase. The polynuclear neutrophiles are usually 
relatively diminished. In this form there appears a new variety of cell, de¬ 
rived from the marrow of the bones, and known as the myelocyte. These cells 
are large and contain a single nucleus, but the protoplasm is finely granular and 
does not stain well with acid coloring matters, resembling in this regard the 
neutrophiles. 

In lymphatic lenkcemia the ratio of white to red corpuscles rarely exceeds 
I : io. The increased number of colorless corpuscles is due to the lympho¬ 
cytes, which may form 93 per cent, of the total number of white cells. Eosin- . 
ophiles and red nucleated cells are rare, and myelocytes do not occur. 

In mixed forms of leukaemia the blood-condition may deviate from either 
of these classical types. 

The accurate study of stained blood-specimens is highly important for diag¬ 
nostic purposes in obscure cases. 

The spleen is usually much increased in size, weighing 
from two to eighteen and a half pounds. The enlargement is 
due to a true hypertrophy of all its constituents. In acute 
cases the spleen is soft and may even rupture. In pro¬ 
tracted cases the organ becomes firmer and the capsule is 
often thickened and adherent to surrounding structures. 
On section hemorrhages may be found in its substance, and 
there may be seen grayish-white areas which consist of 
aggregations of lymphoid cells. 

The lesions in the bone-marrow are usually associated with 
the splenic enlargement. A pure form of medullary or 
myelogenous leukaemia is exceedingly rare. The marrow, 
which is yellowish or even purulent in appearance, contains 
many lymphoid and nucleated red blood-cells. 

The lymphatic glands may be involved alone (lymphatic 
leukaemia) or in connection with the splenic and medullary 
lesions. The histological change consists of hyperplasia of 
the glandular tissue. The glands are enlarged and soft, but 
are freely movable and do not mat together. In many cases 


LEUKEMIA. 


Plate 22 . 



Blood stained with Ehrlich’s “triple stain ” of acid fuchsin, methyl-green, and orange-G; 
drawn with the camera lucida from normal blood (Osier, in American Text-Book of Tie 
Theory and Practice of Medicine)', a, red corpuscles; b , lymphocytes; c, large mono¬ 
nuclear leucocytes ; d, transitional forms ; e, neutrophilic leucocytes with polymorphous 
nuclei (polynuclear neutrophiles) ; f, eosinophilic leucocytes. 




LEUKEMIA. 


7 25 


the glands remain perfectly normal. The liver is usually 
increased in size, from a diffuse infiltration of lymphoid cells. 
New growths composed of lymphoid cells may be found in 
various parts of the body, especially in the tonsils, intestinal 
glands, liver, kidney, retina, lungs, and pleura. The hem¬ 
orrhagic tendency of the disease is shown by hemorrhages 
in various parts of the body, especially under the skin, under 
the serous and mucous membranes, and in the retina. 

Symptoms. — 1. There are regularly present anaemic 
symptoms resembling those of pernicious anaemia, so that 
a detailed description is not necessary. Nervous symptoms, 
however, are not usually marked. CEdema of the feet and 
general dropsy are commonly present. 

2. Hemorrhagic symptoms may be slight or may lead to 
a fatal issue. Hemorrhages may occur from any of the 
mucous surfaces or into the retina, while death may result 
from cerebral hemorrhages. The most frequent hemorrhages 
arise from the nose, stomach, intestines, lungs, and kidney. 

3. There may be an irregular fever as in pernicious 
anaemia. Rare cases of acute leukaemia are encountered, 
in which a continuous temperature of 103° or 104° F. is 
observed. These acute cases may be mistaken for typhoid 
fever unless blood-examination be made. 

4. Splenic tumor is readily appreciated by palpation. 
The spleen may extend to or beyond the umbilicus. The 
free edge is sharp and notched. In acute cases there may be 
pain and tenderness over the spleen, so that, in connection 
with its enlargement, abscess of the organ may be suggested. 
Rupture of the spleen in acute cases has occurred. In pro¬ 
tracted cases no symptoms are caused by the splenic tumor 
except those due to its increased size and weight. 

5. Changes in the marrow rarely give rise to clinical 
symptoms. Exceptionally there is pain in the bones. If 
the sternum be affected, it may be tender on pressure. 


72 6 MANUAL OF THE PRACTICE OF MEDICINE. 

6. Lymphatic enlargements do not occur in all cases. 
More rarely the lymph-glands are affected alone, with the 
changes in the blood; to this form the term “ lymphatic 
leukaemia ” has been given. These cases usually run a rapid 
course with fever or hemorrhages. The glands enlarge, but 
seldom present the same large bunches as in Hodgkin’s dis¬ 
ease. Pain is rare, the glands usually giving rise to no 
symptoms except those caused by pressure. The super¬ 
ficial glands are usually first involved, next in frequency the 
retroperitoneal and mesenteric glands. Enlargement of 
the abdominal glands may often be appreciated by pal¬ 
pation. 

7. Leukaemic new growths may be discovered in the 
tonsils, retina, or liver. Leukaemic deposits in the liver 
may give the symptoms of peritonitis. 

8. In males persistent priapism may occur; it may be the 
first symptom of the disease. 

9. The urine may be albuminous; uric acid is usually 
increased. 

The diagnosis is to be made upon the results of blood- 
examination. Mild degrees of leukaemia may be differen¬ 
tiated from excessive leucocytosis by the fact that in the latter 
the polynuclear neutrophiles are alone increased. The 
diagnosis from Hodgkin’s disease can readily be made by 
the blood-examination. 

Prognosis.—The course of the disease is progressive, 
although through appropriate treatment there may occur 
periods of temporary improvement. Acute cases terminate 
fatally within a few months; the less rapid forms terminate 
at the expiration of one or two years. Death may be due 
to anaemia, exhaustion, fatty degeneration of the heart, or 
hemorrhage. 

The treatment is practically that of pernicious anaemia. 
Iron may be given, but any great amount of improvement 


PSE UD OLE UR EE MIA . 


727 


from its use is not to be expected. Quinine should be 
given to malarial cases, and potassium iodide and mercury 
should be ordered if the patient be syphilitic. Arsenic is 
the drug usually employed, and its use is frequently fol¬ 
lowed by brilliant although temporary results; to be of 
service, however, the drug must be pushed with due precau¬ 
tion until large doses are reached. During treatment by 
arsenic the number of the white cells may be much reduced. 

Splenic remedies have been tried, but they are not 
serviceable. Faradism, injections of ergotine and of qui¬ 
nine, and the use of piperin and of oil of eucalyptus have 
been recommended. Extirpation of the spleen has been 
performed, with a mortality of 95 per cent. Surgical opera¬ 
tions are extremely dangerous in leukaemia, owing to the 
liability of uncontrollable hemorrhage. 

PSEUDO-LEUKEMIA. 

Etiology and Synonyms. —The cause of pseudo-leu¬ 
kaemia is obscure, but of late the view is gaining ground 
that the condition is an infectious process, and that pseudo¬ 
leukaemia really should be assigned to the group of infec¬ 
tious tumors. The disease is more frequent in males than 
in females, in the proportion of 3 : 1. It occurs at any age, 
but two-thirds of the cases are observed in those under 
forty years. In some cases the development of the disease 
has been preceded by inflammatory conditions of any group 
of lymphatic glands. Synonyms: Hodgkin’s disease; 
Lymphatic anaemia; Adenia; General lymphadenoma; 
Pseudo-leucocythaemia; Malignant lympho-sarcoma. 

Pathology. —The lymphatic glands undergo enlargement. 
Histologically the process consists of an increase of the 
lymphoid cells, with or without increase of the reticulum. 
At first the glands are soft and elastic; they may become 
firm and hard. Isolated and freely movable at first, the 


728 MANUAL OF THE PRACTICE OF MEDICINE. 


glands tend finally to become fused together to form 
large lobulated tumors surrounded by a fibrous capsule. 
The new growth of lymphatic tissue may even extend 
beyond the capsule to involve neighboring structures. 
Suppuration of the superficial glands is not uncommon. 
The glands are usually affected in the following order of 
frequency; the cervical, axillary, inguinal, mediastinal, 
retroperitoneal, and mesenteric groups. 

The spleen is enlarged in three-fourths of the cases, but 
the increase is rarely so marked as in leukaemia; in one- 
half the cases grayish-white tumors are found in its sub¬ 
stance ; they consist of lymphoid cells and a connective- 
tissue reticulum. The lymphoid cells of the bone-marrow 
may be increased in number, often to such an extent that 
the marrow resembles pus in its appearance. 

Secondary growths of lymphatic tissue may occur in any 
part of the body, especially in the tonsils, in the lymphoid 
tissue at the base of the tongue, in the liver, spleen, kidneys, 
lungs, pleura (causing fibrino-serous effusion), spinal cord 
(causing paraplegia), and in the skin. The ovaries, testicles, 
and dura mater may also be the seat of new lymphatic 
growths. 

The blood shows the regular changes of anaemia. 
Poikilocytes and nucleated red cells are not present to any 
considerable extent. Lencocytosis docs not normally occur 
in pseudo-leukaemia, but cases occur, occupying a middle 
ground between Hodgkin’s disease and lymphatic leu¬ 
kaemia, in which the white cells are increased in number 
and in which the lesions of a pure lymphatic leukaemia 
may ultimately develop. Some of these cases occur in 
children under two years of age. 

Symptoms are due (i) to anaemia, (2) to the enlargement 
of the lymphatic glands, and (3) to the secondary lymphatic 
growths. 


PSE UD O- L E UK EE MI A. 


7 2 9 


1. The ancemia gives rise to the regular symptoms of that 
condition. The pallor, hemorrhages, oedema, dyspnoea, 
and the cardiac and cerebral symptoms are like those seen 
in pernicious anaemia, and need not be again described. 
Pigmentation of the urine, however, does not occur in 
Hodgkin’s disease. The anaemic symptoms may precede 
or follow those due to the glandular enlargements. The 
temperature is usually irregularly elevated even during the 
earlier stages of the disease. The fever may be continuous 
or recurrent. Remarkable ague-like paroxysms may occur, 
separated by periods of normal temperature. The duration 
of the febrile paroxysms may be weeks or months. 

2 . The glandular sivellings are frequently the first symp¬ 
toms noticed. The glands on one side may be involved 
alone, but later the swellings become symmetrical. At first 
it may be impossible to exclude syphilitic or tubercular dis¬ 
ease ot the glands; but later, when large bunched tumors 
foi m, the diagnosis is usually easy. Marked variations in 
the size of the glands may be observed from time to time. 
In the latter stages the skin may be involved and ulcerated. 
Enlarged retroperitoneal glands may reach such a size that 
large abdominal tumors are formed. Besides the disfigure¬ 
ment caused by the glandular tumors, important symptoms 
may arise from their pressure on neighboring structures. 
The cervical glands may press upon the trachea and may 
necessitate tracheotomy. Enlargement of the mediastinal 
glands may cause pressure upon the trachea, oesophagus, 
bronchi, vena cava, and aorta. Alarming cardiac disturbance 
may arise from compression of the vagus. The enlarge¬ 
ment of the abdominal glands may cause abdominal pain ; 
they may press upon the portal vein (causing acites and 
portal obstruction) or upon the common bile-duct (causing 
persistent obstructive jaundice). Pressure upon the adrenals 
or upon the splanchnic nerves may be followed by bronzing 


730 MANUAL OF THE PRACTICE OF MEDICINE. 


of the skin. The axillary glands may press upon the 
brachial or axillary veins (causing swelling of the arm) or 
upon the brachial plexus (causing numbness, tingling, pain 
along the course of the nerves, or paralysis). The enlarged 
glands in the pelvic and iliac regions may cause sciatic pain 
and swelling of the leg. Lymphatic growths in the liver 
and the spleen are regularly followed by an increase in size 
of these organs. 

3. New lymphatic growths in other parts are followed by 
the regular symptoms of small tumors in the affected struc¬ 
tures. 

The diagnosis from leukaemia is to be made by the 
blood-examination, there being in Hodgkin’s disease no in¬ 
crease in the number of the white cells. The occasional 
merging of pseudo-leukaemia into lymphatic leukaemia 
should not, however, be forgotten. The diagnosis from 
tubercular adenitis is usually rendered easy by the presence 
of other foci of tubercular disease in the latter condition. 
Tubercular adenitis usually involves the submaxillary glands, 
whereas in Hodgkin’s disease the glands along the borders 
of the sterno-mastoid muscle are the glands first to be 
involved. Suppuration is common to tubercular glands, 
uncommon to those of Hodgkin’s disease. 

Prognosis.—With rare exceptions Hodgkin’s disease 
ultimately ends fatally. The course of the disease is fre¬ 
quently marked, however, by more or less prolonged 
periods of improvement. Acute cases may run a course of 
several months ; the more protracted cases may extend over 
two or three years. Death results from debility and 
anaemia, from hemorrhage, from the mechanical pressure of 
the lymphatic tumors, or from intercurrent disease. 

Treatment is mainly that of pernicious anaemia. Arsenic 
is to be given until the point of tolerance is reached. Phos¬ 
phorus has also been recommended, but it is of doubtful 


ADDISON'S DISEASE. 


7 3i 


utility. The internal use of Lugol’s solution of iodine in 
from 5- to io-drop doses after meals has been recommended. 
In early cases, in which only a few glands are enlarged, 
these glands may be removed by surgical operation. Re¬ 
moval of the glands may also be resorted to in case of 
severe pressure-symptoms. 

ADDISON’S DISEASE. 

Etiology. —Addison’s disease is more frequent in men 
than in women, and usually occurs in middle life, although 
no age is exempt. About the causation of the disease there 
is much doubt. Two theories exist: (1) That the disease 
is due to loss of function of the suprarenal capsules. 
(2) That the disease is due to irritation of the abdominal 
sympathetic plexus, usually owing to disease of the nerves, 
the ganglia, or the adrenals. In other cases a functional 
nerve-disturbance must be supposed to exist. 

Pathology.—In 88 per cent, of all cases the adrenals are 
found diseased. In the vast majority of cases the lesion in 
the adrenals is tubercular, the capsules being converted into 
masses of fibrous tissue and cheesy matter. In other 
cases the adrenals are found atrophied, absent, or the seat 
of malignant tumors. Against the theory that Addison’s 
disease is due to loss of function of the suprarenal capsules 
through disease are the following facts: (1) In 17 per cent, 
of all cases of Addison’s disease the adrenals are found 
to be normal. (2) Every variety of adrenal lesion has 
occurred without giving rise to the symptoms of Addison’s 
disease. Owing to improved technique in nerve-staining, 
there are found an increasing number of cases of Addison’s 
disease in which lesions are found in the sympathetic nerve- 
structures in the abdomen. Of the 30 cases most recently 
examined, 27 showed sympathetic nerve-lesions. The 
ordinary lesions found in the ganglia and nerve-fibres 


732 MANUAL OF THE PRACTICE OF MEDICINE. 

consist of degeneration, congestion, hemorrhages, and in¬ 
filtration by leucocytes or new connective tissue. The 
blood shows the changes common to anaemia. The heart 
maybe fatty; it is seldom enlarged. The liver shows no 
essential lesion. The spleen may be somewhat increased in 
size. Tubercular changes are often found in various parts 
of the body if tubercular disease of the adrenals be present. 

Symptoms.—Four cardinal groups of symptoms appear: 
(i) prostration, (2) heart weakness, (3) gastro-intestinal symp¬ 
toms, and (4) bronzing of the skin. 

1. Prostration is shown by the early appearance of intense 
languor both of body and of mind. The patient becomes 
weak, dull, apathetic, listless, and peevish. The symptoms 
of prostration are constant and progressive. 

2. Heart weakness is attended by frequent syncopal at¬ 
tacks, any one of which may be fatal. The pulse is feeble 
and rapid. The poor condition of the circulation induces 
the symptoms of cerebral anaemia, which usually are well 
marked. 

3. Gastro-intestinal symptoms are almost constant. Nausea 
and vomiting may, with the prostration, appear as initial 
symptoms. The vomiting, which is not usually influenced 
by diet, cannot be accounted for by any lesion found in the 
stomach, but seems to be of nervous origin. The vomiting 
occurs in violent paroxysms and becomes more distressing 
as the disease progresses. Diarrhoea is twice as frequently 
observed as constipation. 

4. The bronzing of the skin is usually observed after the 
constitutional symptoms have lasted for some little time. 
In other cases it is the first symptom observed. The pig¬ 
mentation of the skin usually begins in the exposed portions 
of the body, as the face and the hands, or in areas exposed 
to friction of the clothing, or in places which are normally 
pigmented, as about the nipples. The color varies from a 


TUBERCULOSIS OF THE LYMPH-GLANDS. 


733 

yellow to a brown or even a black. The pigmentation may 
at first occui in scattered areas, but finally tends to become 
diffused, so that the patient may resemble a mulatto. Simi¬ 
lar discoloration may be found in the mucous membrane of 

the lips, gums, and tongue. Internal pigmentation does not 
usually occur. 

Among the remaining symptoms to be enumerated, the most 
important are pain and tenderness in the lumbar or epigas¬ 
tric regions ; these symptoms occur in one-third of the cases. 
In the last stages of the disease the patients become ex¬ 
tremely feeble and may develop stupor, delirium, coma, 
or general convulsions. Death occurs from asthenia or 
from syncope. In a few acute cases the disease runs a 
course with fever, vomiting, diarrhoea, and intense exhaus¬ 
tion, and before the pigmentation appears the diagnosis may 
be impossible. 

Prognosis. —Recovery is practically unknown. Acute 
cases may terminate within a few months. The average 
duration is about one year, but cases are on record in which 
the symptoms continued as long as ten years. 

Treatment is symptomatic, as for the disease itself no 
curative treatment is known. The patient should be guarded 
from causes leading to syncope, and anaemic conditions 
should be controlled by iron and arsenic. The vomiting 
may be alleviated by bismuth, creosote, hydrocyanic acid, 
or codeia. Purgatives should be given with caution, as they 
may induce an exhausting diarrhoea. 

TUBERCULOSIS OF THE LYMPH-GLANDS 

(SCROFULA). 

Etiology. —Scrofula is tubercle, and the etiology of 
scrofula is therefore that of other tubercular infections. 
Tubercular infection of lymphatic glands is favored by 
previous adenitis, so that children with catarrhal inflamma- 


734 MANUAL OF THE PRACTICE OF MEDICINE . 

tions of the mucous membranes that excite adenitis of the 
neighboring lymphatic glands seem to be especially sub¬ 
ject to subsequent lymphatic tuberculosis. 

The pathology of scrofula is that of tubercular foci, 
which are usually localized in certain groups of glands 
and show a tendency to spontaneous healing. In many 
cases suppuration of the infected glands occurs, espe¬ 
cially with tubercular glands in the neck. In these in¬ 
stances the pus is usually sterile, and it is not known 
whether the suppuration is excited by the tubercle bacilli 
and their products or by a mixed infection of pus-or¬ 
ganisms. An unhealed focus of tubercular adenitis may 
at any time discharge bacilli into the blood-vessels or the 
lymph-vessels; it is said that three-quarters of the cases 
of acute miliary tuberculosis originate in this way. 

Symptoms.—i. General tuberculous lymphadenitis is a 
rare condition, and usually occurs in the negro race. The 
lymph-glands throughout the body are the seat of a diffuse 
tubercular infiltration. Acute cases resemble clinically 
Hodgkin’s disease, but there is apt to be more fever. 

2. Local Tuberculous Lymphadenitis. — (a) Cervical .—This 
form is frequently seen, especially in tenement-house and 
asylum children and in the negro race. The submaxillary 
glands are usually the first to be involved, and subsequently 
the cervical chains of glands become infected. The glands 
may remain isolated and mobile, but they tend to become 
fused so as to form large knobby tumors. Suppuration is 
common. For the details of this affection the reader is 
referred to works on surgery. 

(b) Bronchial .—The bronchial glands are extremely sub¬ 
ject to infection, and they may be involved with or without 
local lesions in the lung. Acute miliary tuberculosis is apt 
to result. (For details see Miliary Tuberculosis and Bron¬ 
cho-pneumonia.) 


TUBERCULOSIS OF THE LYMPH-GLANDS. 


735 

if) Mesenteric (Tabes Mesenteric a ).—In this form the 
mesenteric and retroperitoneal glands are enlarged and 
tubercular. They may suppurate, or they may become 
encapsulated and infiltrated by lime-salts. Mesenteric 
tuberculosis may be primary or may complicate tubercular 
disease of the intestines. 

The treatment of tubercular adenitis is that of tuber¬ 
culosis in general. Cervical tubercular glands may be 
removed. 


VIII. DISEASES OF THE NERVOUS SYSTEM. 


i. DISEASES OF THE MEMBRANES OF THE BRAIN. 

(a) Diseases of the Dura Mater. 

ACUTE EXTERNAL PACHYMENINGITIS. 

Etiology.—Pachymeningitis is regularly secondary to 
injuries and diseases of the cranial bones and to suppura¬ 
tive disease of the middle ear and of the mastoid cells. 

Pathology.—The dura is thickened by a purulent infil¬ 
trate ; the products of inflammation collect between the 
dura and the skull, forming a circumscribed abscess. The 
lesion is usually localized over one cortex. The inflamma¬ 
tion may extend to the pia mater or to the venous sinuses. 

The symptoms are usually obscure. Pain is usually 
referred to the seat of the lesion. Septic symptoms develop, 
and compression-symptoms may result in hemiplegia if the 
motor area be pressed upon. 

The prognosis is good if the treatment be scientific and 
if the pia and the venous sinuses be not involved. 

The treatment consists in trephining and draining the 
abscess-cavity. 

ACUTE INTERNAL PACHYMENINGITIS. 

Etiology. —Pachymeningitis interna is secondary to in¬ 
flammation of the external surface of the dura, or compli¬ 
cates erysipelas, Bright’s disease, pyaemia, pneumonia, puer¬ 
peral fever, and the exanthemata. 

736 



CHRONIC INTERNAL PACHYMENINGITIS . 737 

Pathology.—The inner surface of the dura is covered 
with fibrin and pus or with pus alone; the thickness of the 
dura is not usually involved. The inflammation is apt to 
extend to the pia and to the venous sinuses. The purulent 
exudation is usually circumscribed over the cortex. 

The symptoms resemble those of a localized purulent 
meningitis. In the complicating cases the symptoms may 
be so obscured by those of the primary disease that the 
diagnosis is rendered obscure. 

The prognosis is not good, owing to the liability to 
meningitis and thrombosis of the cerebral sinuses. 

The treatment is that of meningitis. 

CHRONIC INTERNAL PACHYMENINGITIS. 

Etiology and Synonyms.—The disease is usually found 
in males over fifty years of age; it occurs in connection 
with insanity and degenerative diseases of the brain. Al¬ 
most all the subjects are markedly alcoholic, and the disease 
is one almost exclusively of tramps and almshouse inmates. 
Synonyms : Hemorrhagic pachymeningitis ; Haematoma of 
the dura mater. 

Pathology.—The disease is characterized by the growth 
of a new membrane upon the dura, usually involving a small 
area over one cortex. In the earlier stages this membrane 
resembles a brownish-red staining of the dura, and consists 
of large, thin-walled blood-vessels supported by a delicate 
connective-tissue framework. From these blood-vessels 
hemorrhages occur, constituting the principal feature of the 
disease. In the later stages the dura is thickened over the 
affected area by dense fibrillated connective tissue, and upon 
its inner surface the original membrane is found as already 
described. The dura may be from half an inch to an inch 
thick, and thus the brain becomes slowly compressed; 
the compression of the brain is further increased by hemor- 


47 


738 MANUAL OF THE PRACTICE OF MEDICINE. 

rhage between the dura and the pia, which may occur at any 
time. 

The symptoms are due to slow and to sudden brain- 
compression. 

Slow Compression .—Headache is prominent, constant, and 
usually localized. There are loss of memory and increasing 
stupidity. The gait is shambling, slow, and unsteady, but 
paralysis and ataxia are not observed. The speech becomes 
slow, faltering, and scanning. One or both pupils may be 
contracted. In the earlier stages 01 the disease these symp¬ 
toms are not marked. 

Sudden compression is caused by meningeal hemorrhages. 
The patient will become unconscious, with or without pre¬ 
ceding convulsions, and will develop hemiplegia (see Menin¬ 
geal Hemorrhage). The hemorrhage may occur sponta¬ 
neously or after exertion, or after a blow or an injury to the 
head. In the latter instance the disease possesses great 
medico-legal interest. The hemorrhage may occur early 
in the disease and may be the initial symptom. 

Prognosis. —The disease is slow in its progress, extend¬ 
ing over years. Rare cases of recovery have been repoited. 
Death usually occurs from degeneration of the brain with 
insanity, or from hemorrhage. 

Treatment.—As the diagnosis from syphilitic meningitis 
cannot in all cases be made, potassium iodide should be 
given in full doses. This treatment, however, is of no ser¬ 
vice in non-syphilitic pachymeningitis. The treatment of 
the disease is chiefly prophylactic. Quiet, easy employ¬ 
ment, and the avoidance of severe bodily exertion should 
be enforced, to lessen the chance of meningeal hemorrhage. 

SYPHILITIC PACHYMENINGITIS. 

This disease will be considered under the heading of 
Syphilitic Disease of the Brain-membranes. 


TUBERCULAR MENINGITIS. 


7 39 


(b) Diseases of the Pi a Mater. 

The pia mater may be the seat of a tubercular, a non- 
tubercular, and a syphilitic inflammation. Its inflammations 
are called “ meningitis ” or “ leptomeningitis.” 

TUBERCULAR MENINGITIS. 

Etiology. —In young children tubercular meningitis is 
regularly only part of an acute general tuberculosis. For 
the etiology see the latter disease. 

In adults tubercular meningitis is usually a local inflam¬ 
mation secondary to some pre-existing tubercular dis¬ 
ease. In some adults with acute general tuberculosis 
the lesions of tubercular meningitis may be found at the 
autopsy, but clinical symptoms during life are not usually 
observed in these cases. 

Tubercular meningitis is most common in children be¬ 
tween two and seven years of age. In adults the disease is 
rare after the twenty-fifth year. The attack may seem to 
be induced by some exciting cause, as a blow, a fall, or 
exposure to a hot sun. 

Pathology. —Upon removing the skull-cap the brain 
appears too large and the convolutions are flattened. The 
tubercles appear as small grayish points, occasionally with 
cheesy centres. The tubercles are most abundantly found 
along the course of the blood-vessels and in the sulci. They 
may be confined to the base (hence the name “ basilar men¬ 
ingitis ”) or they may be more uniformly distributed. The 
pia about the tubercles is thickened by serum and by cel¬ 
lular infiltration. Properly speaking, there should be no 
purulent exudate, but a fibrino-purulent exudate is not 
uncommon from a “ mixed infection.” The cortex is 
oedematous and is infiltrated with cells. In children the 
ventricles are regularly distended with clear or turbid serum, 
and the walls of the ventricles are studded with tubercles 


740 MANUAL OF THE FT AC TICE OF MEDICINE. 

(“ acute hydrocephalus ”). This distention may be so great 
that the septum between the lateral ventricles will rupture, 
and great compression of the brain from within outward will 
ensue. In adults the distention of the ventricles is less fre¬ 
quent. In all cases tubercular inflammations are seen in 
other parts of the body. 

The symptoms may be classically divided into four 
groups: 

Prodromal Symptoms—The child is irritable, restless, and 
disinclined to play. Causeless vomiting is a symptom which 
in children is suggestive of incipient meningeal inflamma¬ 
tion. 

Symptoms of Brain-irritation .—The child may be taken 
with convulsions or a chill. Fever develops and runs an 
irregular course. The temperature may vary between ioo° 
and 103° F. with irregular remissions; more rarely a fever 
of 104° to 105° F. is encountered. The temperature gives 
no guide to the diagnosis, nor does it indicate the actual 
severity of the disease. Headache becomes severe, and the 
special senses are so hyperaesthetic that the child becomes 
intolerant of light or noise, and the hyperaesthesia of the 
skin may render any handling of the patient extremely pain¬ 
ful. There is rigidity and retraction of the back of the neck ; 
the muscles generally are rigid and resist passive motion, 
and the general attitude is one of general flexion which is 
quite characteristic. Convulsive movements or automatic 
motions are common. Mild or violent delirium develops, 
alternating with periods of stupor in which the child may 
moan or give vent to the shrill “ hydrocephalic cry.” The 
pupils are usually contracted. The pulse varies between 
no and 120. Vomiting attacks occur without nausea, and 
are not influenced by the taking of food. The bowels are 
usually obstinately constipated. The abdomen is retracted 
and “ boat-shaped.” 


ACUTE NON-TUBERCULAR MENINGITIS. 741 

Symptoms of brain-compression next appear, and are due 
not only to the thickening of the pia, but also to the disten¬ 
tion of the ventricles. The child becomes dull and apathetic. 
The special senses are blunted. Stupor succeeds the delirium 
and merges into coma. The automatic motions of the hands 
and feet may continue, or there may be evident paralysis of 
certain groups of muscles, of which paralyses squint is the 
most easily recognized. The pulse may now become slowed 
to 90, 80, or even 60 in the minute. This characteristic 
slowness of the pulse, however, may not be marked in young 
children. Irregularity of the pulse is frequently observed. 
The coma becomes profound, the sphincters relax, paralysis 
becomes more evident; the pulse during the last stages of 
the disease becomes rapid and feeble, and the breathing 
becomes irregular and may assume the Cheyne-Stokes 
variety. Death occurs from depression of all the vital 
functions. 

Not all cases, however, run this classical course. The 
symptoms of irritation and of compression may be vari¬ 
ously admixed, according to the intensity of the inflam¬ 
mation in various portions of the pia mater. Some young 
children are seized at the onset with convulsions, which may 
be repeated; the child becomes stupid and drowsy, moans as 
if in pain, and develops irregular fever; the rhythm of the 
respirations becomes disturbed, and coma precedes a fatal 
issue. In adults, owing to the less frequent movement of 
the ventricles, the compression-symptoms are less marked. 

The prognosis is uniformly bad. 

The duration of the disease is from one to four weeks. 

The treatment is that of acute non-tubercular meningitis. 

ACUTE NON-TUBERCULAR MENINGITIS. 

Etiology. —Meningitis is regularly due to germ-infection 
of the pia mater. The inflammation of the pia mater occurs 


742 MANUAL OF THE PRACTICE OF MEDICINE. 

as the characteristic lesion of epidemic cerebro-spinal menin¬ 
gitis. 

Cases of secondary pus-infection occur more commonly, 
the germs infecting the meninges (i) by direct extension or 
(2) through the arteries. 

1. By direct extension , following inflammation or injury of 
the bones of the skull, of the dura mater, or of the orbital 
cavity. The most frequent cause is necrosis of the petrous 
portion of the temporal bone from middle-ear disease. The 
germs may travel along the nerve-roots during the course 
of facial erysipelas, or a phlebitis arising from suppuration 
of the orbit or cheek may infect the cavernous sinus and 
thus spread to the pia. 

2. Through the Arteries. —Infectious emboli may occur in 
the course of pyaemia, abscess of the lung, and malignant en¬ 
docarditis. Bacterial infection also occurs during the course 
of certain infectious diseases, especially pneumonia, ery¬ 
sipelas, typhoid fever, rheumatism, and the exanthemata. 
Infection is favored by Bright’s disease and gout. The con¬ 
gestion following sunstroke predisposes to meningitis. 

Pathology.—Two anatomical forms are found, which 
during life give rise to the same clinical symptoms : 

1. Cellular Meningitis. —The pia is congested, dry, and lus¬ 
treless. The substance of the pia is the seat of a cellular 
infiltration. There is no purulent exudate. This form is 
analogous to the cellular form of peritonitis in peritoneal 
septicaemia. 

2. Exudative Meningitis. —There is an exudation of fibrin, 
serum, and pus into the thickness of the pia, more rarely 
appearing upon its free surface. In children and in young 
adults the lining of the ventricles becomes inflamed and the 
ventricles become distended with turbid serum. The pia 
mater covering the spinal cord may be involved by direct 
extension. The locality of the meningitis varies. In 


ACUTE NON-TUBERCULAR MENINGITIS. 


7 43 


pneumonia and in malignant endocarditis the process is 
usually bilateral and limited to the cortex ; with middle-ear 
disease the lesion is over the temporo-sphenoidal lobe on 
one side ; in other cases the base alone may be involved. 
In children, should the patient recover from the meningitis, 
the ventricles may remain distended for some time. 

The symptoms depend largely upon the charactei of the 

original disease. 

i. If the meningitis follow middle-ear disease, the symp¬ 
toms of meningitis are well developed and resemble those 
of the tubercular or the epidemic form, so that a further 
description is unnecessary. The diagnosis from tubercular 
meningitis is to be made by attention to the following 
points: 


Tubercular Meningitis. 
History of tuberculosis. 

No apparent cause. 

Longer prodromal period. 
Longer course. 

o 

Presence of tuberculosis in 
the lungs, etc. 

Heredity in 20 per cent. 


Simple Meningitis. 
History of ear disease, etc. 
Cause evident. 

Short prodromal period. 
Short course. 

No tuberculosis. 

No heredity. 


2. If the meningitis complicate severe infectious disease, 
the symptoms may be obscured by those of the original 
disease. Retraction of the head and paralyses may consti¬ 
tute the only suggestive symptoms. Facial paralysis and 
squint are usually the most evident. The pulse may or 
may not become slower, but it usually becomes irregular. 
Irregularities of the rhythm of respiration are usually 
observed. It may be impossible to differentiate between 
pnuemonia in children with cerebral symptoms and pneu¬ 
monia complicated by meningitis. 

The duration is about a week, but the disease may con¬ 
tinue for from two to four weeks. 


744 MANUAL OF THE PRACTICE OF MEDICINE. 

The prognosis is bad, yet a number of patients recover. 

Treatment. —The patient should be kept free from noise 
and lisrht. The continual use of the ice-cap throughout 
the disease is frequently of service, and should always be 
employed. Leeches should be applied behind the ear in 
robust cases, but depletion in the latter stages of the disease 
is not to be advised. Blisters to the occiput add to the dis¬ 
comfort of the patient and do no good. Calomel and mag¬ 
nesium sulphate should be given at the outset, in such 
doses as will act on the bowels and reduce the meningeal 
congestion. Ergot is advised during the earlier stages, to 
reduce congestion. Potassium iodide in 5- to 10-grain doses 
is employed as a routine treatment, but its use is theoretical. 
The restlessness and headache are to be controlled by 
opium, phenacetine, chloral, bromide of sodium, and sul- 
phonal. For the tubercular form the head may be shaved 
and covered with iodoform ointment; for this treatment 
good results have been claimed. Should meningitis follow 
middle-ear disease or suppurative disease of the dura, local¬ 
ized trephining and drainage should be practised. 

To avoid meningitis prophylactic treatment should be 
directed toward the careful cleansing of the ear in suppura¬ 
tive otitis media, the opening and draining of abscesses of 
the mastoid cells, and the antiseptic treatment of suppura¬ 
tive processes about the cheeks and the orbit. 

SYPHILITIC MENINGITIS. 

(See Syphilis of the Brain.) 

CHRONIC MENINGITIS. 

Etiology and Synonym.—The disease is one of middle 
life, and is most commonly seen in those who have led a 
life of privation and exposure. It is common in tramps and 
in the inhabitants of almshouses. Chronic alcoholism and 


MEN INGE A L HEMORRHA GE. 


745 


cerebral endarteritis seem to lead to the disease. Chronic 
meningitis may complicate fractures or inflammation of the 
cranial bones, chronic pachymeningitis, chronic Bright’s 
disease, chronic degenerations of the brain, and slow-grow¬ 
ing cerebral tumors. Synonym : Chronic leptomeningitis. 

Pathology. —The pia mater is thickened, opaque, cedem- 
atous, and infiltrated with cells. There may be adhesions 
between the pia and the dura. The brain-cortex may be 
softened or sclerotic. The ventricles may be distended with 
clear serum, and the ependyma lining them may be thick¬ 
ened and rough. The meningitis may be localized at the 
base or the cortex of the brain. 

The symptoms are those of slow compression ; they re¬ 
semble those of chronic pachymeningitis except that hemor¬ 
rhages do not occur. 

Prognosis. —The disease is chronic in its course, extend¬ 
ing over years, but recovery cannot be expected. 

Treatment. —Syphilitic meningitis should be excluded 
by a conscientious trial of mercury and of potassium iodide 
in full doses. Otherwise the treatment is symptomatic. 

MENINGEAL HEMORRHAGE. 

Hemorrhage may occur between the dura mater and the 
bones of the skull, and between the dura and the pia mater. 

Hemorrhage between the Dura Mater and the 
Bones of the Skull. — Etiology. —These hemorrhages are 
regularly due to violence, either by concussion separating 
the dura from the cranial bones and lacerating the middle 
meningeal artery, or by fracture of the cranial vault. 

The symptoms are those of shock, laceration and com¬ 
pression of the brain, followed by the symptoms of menin¬ 
gitis. Although these cases are of surgical rather than of 
medical interest, they are important to the physician, owing to 
the unpleasant results that follow an erroneous diagnosis. A 


746 MANUAL OF THE PRACTICE OF MEDICINE. 

man whose breath is alcoholic may be found unconscious in 
the street with a scalp-wound. The case is regarded as 
one of alcoholism, but the coma deepens, the temperature 
rises, and the patient dies. At the autopsy there is found a 
fracture of the skull with laceration of the middle cerebral 
artery and meningeal hemorrhage. 

Treatment. —In suspected cases incision should be made, 
exposing the site of probable fracture. When the diagnosis 
is made, trephining and removal of the clots should at once 
be resorted to. 

Hemorrhage between the Dura Mater and the Pia 
Mater.— Etiology. —This form of meningeal hemorrhage 
may occur from—(1) Traumatism ; (2) thrombosis of the 
venous sinuses; (3) in new-born children as the result of 
severe labor or the pressure of forceps; (4) chronic hemor¬ 
rhagic pachymeningitis ; (5) rupture of an aneurysm of one 
of the cerebral arteries; (6) after convulsions in children; 
(7) hemorrhagic diseases. The disease may occur at all 
ages, thus differing from cerebral hemorrhage. 

Pathology, —The hemorrhage may be at the base of the 
brain, at the convexity, or may be more equally distributed. 
Small hemorrhages may ultimately be absorbed, leaving 
haematin staining. It must be remembered that in cerebral 
hemorrhage the blood may rupture through the cortex or 
may leak out by the fourth ventricle and appear between 
the membranes. 

The symptoms vary according to the size, location, and 
cause of the hemorrhage. 

I. Large Clot over One Cortex. —There is sudden coma, 
with stertorous breathing, slow pulse, and abolition of all 
reflexes. There may be hemiplegia or monoplegia, according 
to the size and position of the hemorrhage. Convulsive 
movements of muscles ultimately to be paralyzed may occur. 
The temperature falls to 96° or 97 0 F., but subsequently 


CONGESTION. 


747 


rises to 103° or 105° F. or even higher. The patient may 
die in coma within twenty-four hours, or may die in several 
days with the symptoms of meningitis. Recovery occurs 
only if the clot be small. Small hemorrhages over a con¬ 
vexity may give rise to the symptoms of acute meningitis 
without the occurrence of sudden coma. 

2. Clots over both hemispheres give rise to sudden coma 
and general convulsions, so that the diagnosis from uraemia 
may be one of great difficulty. 

3. Hemorrhage at the base of the brain compresses the 
medulla and leads to death in a few hours. A high ante¬ 
mortem temperature is usually observed in these cases. 

4. Meningeal Hemorrhage of the New-born .—The child 
may be stillborn, or it may be born in asphyxia, from which 
it may die, or from which it may recover, only to die in 
coma with convulsions within a few days. In those who 
live, symptoms of paralysis with or without athetosis, mental 
defects, and epileptic seizures may develop (see Cerebral 
Atrophy of Children). 

The prognosis of meningeal hemorrhage is bad unless 
the clot is small and is situated over the convexity. Re¬ 
covery may be complicated by permanent paralysis (with or 
without convulsive movements) of groups of muscles upon 
the side opposite to the lesion. Death from meningeal 

o 

hemorrhage usually occurs earlier than from cerebral 
hemorrhage. 

2. DISEASES OF THE BLOOD-VESSELS OF THE 

BRAIN. 

CONGESTION. 

Congestion may be active or passive. 

Active JiypereEinia may be due to exposure to the sun, to 
the ingestion of such drugs as alcohol, amyl nitrite, and 



748 MANUAL OF THE PRACTICE OF MEDICINE. 

nitroglycerin, to excessive brain-work, to reflex causes, or to 
fever. 

Passive hypcrcemia results from (i) mechanical obstruc¬ 
tion to the venous return of blood, as with tumors of the 
neck or strangulation; (2) from general venous congestion 
due to heart or lung disease. 

The symptoms are neither characteristic nor constant. 
The active congestion causes headache, a sense of fulness 
and throbbing in the head, and hyperaesthesia of the special 
senses. The face is flushed ; the superficial arteries pulsate 
visibly. Passive hyperaemia gives rise to dull headache, to 
mental slowness, to disturbances of sleep, and to a feeling 
of fulness in the head. Attacks of delirium or unconscious¬ 
ness may attend the severer forms of congestion. 

Treatment. —The patient should be kept quiet, and the 
bowels should be freely moved. Venesection may be in¬ 
dicated in acute congestion of an intense type, and an ice¬ 
cap should be applied to the head. In passive hyperaemia 
the treatment should be directed toward the cause of the 
condition. 

AN2EMIA. 

Anaemia may result from general or local causes. Local¬ 
ized anaemia may be due to vaso-motor constriction, en¬ 
darteritis, or cerebral compression. 

Symptoms. —Acute anaemia, such as results from pro¬ 
fuse hemorrhage, gives rise to confusion of ideas, marked 
dyspnoea amounting to “ air-hunger,” spots before the eyes, 
ringing noises in the ears, a tendency to yawn, nausea, and 
dilated pupils. Convulsions and syncope may occur. Sud¬ 
den death in syncope may result from an intense anaemia 
suddenly induced. 

Chronic anaemia is characterized by vertical headache, 
disturbances of sleep, lack of mental power and concen¬ 
tration. There are spots before the eyes and buzzing in 


CEREBRAL HEMORRHAGE. 749 

the ears. There may be repeated syncopal attacks. The 
symptoms are regularly relieved by lying down. 

The treatment is that of anaemia. 

CEDEMA. 

CEdema may be due (1) to atrophy of the cerebral cortex, 
there being an increase of the cerebro-spinal fluid and 
oedema of the overlying pia: to such a condition the 
term “ wet brain ” has been applied ; (2) to long-continued 
passive congestion; (3) localized oedema occurs about 
tumors and abscesses ; (4) oedema may occur during the 
advanced stages of Bright’s disease. 

The symptoms are obscure, and, in general, are due to 
the disease to which the oedema is secondary. 

CEREBRAL HEMORRHAGE (APOPLEXY). 

Etiology. —Cerebral hemorrhage usually occurs after the 
age of forty, the age of the greatest liability being between 
the seventieth and eightieth years. More rarely the disease 
occurs in children and in young adults. The condition is 
more common in males than in females. An “apoplectic 
habit” has been described—a short, thick-set body, with 
flushed face, prominent color, and short neck, but, as a 
matter of fact, hemorrhage is, if anything, more common 
to those of spare habit. In almost all cases there occurs 
degeneration of the cerebral arteries, rendering them liable 
to rupture. Fatty degeneration, atheroma, or the weaken¬ 
ing of an artery from an embolus may be found, but the 
most frequent cause of hemorrhage is an endarteritis which 
allows of the production of miliary aneurysms, from whose 
rupture the hemorrhage takes place. These miliary an¬ 
eurysms occur with greatest frequency upon the middle cere¬ 
bral artery ; they vary in size up to that of a pin’s head. The 
predisposing causes for the endarteritis are gout, syphilis, 


750 MANUAL OF THE PRACTICE OF MEDICINE. 

alcoholism, and a life of over-work and privation. There 
may be an inherited tendency toward arterial degeneration. 
The exciting cause for rupture is an increased arterial ten¬ 
sion. As high tension so frequently occurs with chronic 
nephritis and hypertrophy of the left ventricle, the associa¬ 
tion of these conditions with cerebral hemorrhage is ex¬ 
ceedingly common. A sudden increase of blood-tension 
may occur from strain, fright, anger, a cold bath, or over¬ 
eating or drinking. In other cases the hemorrhage may 
occur during rest or sleep. 

Cerebral hemorrhage in young adults may be associated 
with congenital lack of development of the aorta and large 
vessels. Hemorrhage may occur during the course of 
hemorrhagic disease, as leukaemia, pernicious anaemia, and 
purpura haemorrhagica, but these hemorrhages are usually 
multiple and have no especial seat of selection. 

Pathology. —Cerebral hemorrhage usually occurs from 
the middle cerebral artery, and involves the internal cap¬ 
sule, optic thalamus, corpus striatum, and the neighboring 
brain-tissue. Next in frequency are hemorrhages into the 
cortex, pons, and cerebellum. The right side is more fre¬ 
quently involved than the left. Should the hemorrhage 
occur near the cortex, the blood may rupture through and 
appear beneath the dura. Rupture into a ventricle may 
also occur. The clot at first is red, soft, and admixed with 
lacerated brain-tissue. Gradually the clot becomes firmer, 
the haemoglobin becomes converted into reddish-brown 
haematoidin, the disintegrated brain-tissue undergoes fatty 
degeneration and absorption, and a connective-tissue capsule 
may form about the hemorrhagic mass. Ultimately there 
may be left a pigmented puckered cicatrix, or a mass of 
softened pigmented tissue with or without a connective- 
tissue wall, or a cyst with brownish fluid contents. The 
torn brain never unites. From the point of laceration sec- 


CE REBRA L HE MO RR HA GE. 


7 51 


ondary degeneration occurs, upward to the cortex if the 
sensoiy tiact be involved, downward in the motor tract as 
far as the anterior motor cells of the spinal cord if the 
lesion involve motor fibres (see Secondary Lateral Scle¬ 
rosis). 

The symptoms depend upon the size, rapidity, and posi¬ 
tion of the hemorrhage. The symptoms are the prodromal, 
those of the attack, and those of the chronic stage. 

Prodromal symptoms , which are due to the cerebral endar¬ 
teritis, consist of headache, dizziness, ringing in the ears, and 
irritability of temper. More characteristic are temporary 
loss of speech, incomplete temporary paralysis of an arm or 
a leg, or temporary and partial blindness. 

Symptoms of the Attack .—The patient, without warning, 
becomes dizzy and falls unconscious. In other cases coma 
may be developed gradually, or may be preceded by forget¬ 
fulness and mental aberration. The face is flushed; the 
arteries of the neck pulsate visibly; respirations are slow 
and stertorous, and may be irregular; the eyes and the 
head are turned toward the side of the lesion (“conjugate 
deviation ”); the pupils vary, but are usually dilated and in¬ 
active; the pulse is full, slow, and of high tension; the tem¬ 
perature at the time of onset falls to subnormal, but within 
twenty-four hours it begins to rise. The more severe the 
hemorrhage, the greater is the initial fall and the higher the 
subsequent rise. Evidences of paralysis may be discovered : 
the mouth may be drawn from the paralyzed side; the 
paralyzed cheek may blow out during respiration more than 
the other cheek, and the naso-labial fold may be obliterated. 
Hemiplegia may be discovered by finding that the affected 
arm and leg drop more “ dead ” than do those of the un¬ 
paralyzed side, and lack their normal “ tone.” The urine 
may contain a trace of albumin or of sugar, even if there be 
no nephritis. 


752 MANUAL OF THE PRACTICE OF MEDICINE. 

Small hemorrhages slowly developing may cause no 
actual coma, but bewilderment and mental confusion are 
commonly observed in these cases. Hemorrhages in the 
cortex or into a ventricle may cause convulsions at the onset, 
but these cases are uncommon. In this condition of coma 
the patient may die, from involvement of the vital functions 
or from hypostatic pneumonia and pulmonary oedema. 

Symptoms of the Chronic Stage .—When the attack does 
not prove fatal, consciousness becomes gradually restored 
and the reflexes return, and it becomes possible to gauge 
the extent of the damage done by the hemorrhage. The 
symptoms of motor paralysis depend upon the extent to 
which the motor tract is lacerated. If the hemorrhage be 
in its usual location, there remains a hemiplegia of the op¬ 
posite side. The muscles, however, are not uniformly par¬ 
alyzed. Those muscles used automatically and in pairs, as 
the muscles of respiration, escape paralysis ; the arm is more 
paralyzed than the thigh, the hand and foot moiethan the 
arm and leg. If recovery ensue, the larger and more auto¬ 
matic muscles improve more rapidly and completely, the 
leg before the arm, the arm before the hand. An “ initial 
rigidity ” of the paralyzed muscles is due to irritation about 
the lesion. An “ early rigidity ” may develop on the second 
or third day and may last for one or two weeks ; this rigidity 
is due to inflammation about the lesion. In early rigidity 
the position of the limbs is one of rest. Late ligidity 
appears after several weeks and is usually permanent. It is 
due to descending degeneration of the motoi tiact (see Sec¬ 
ondary Lateral Sclerosis). The position of the affected 
limb is generally one of flexure. Slow convulsive twitch- 
ings may occur in the paralyzed muscles; this post-hemi¬ 
plegic chorea ” is due to destructive lesions of the optic thala¬ 
mus. During late rigidity the reflexes of the affected limbs 
are greatly exaggerated. Atrophy of the paralyzed muscles 


CEREBRAL HEMORRHAGE. 


753 


does not occur. Facial paralysis occurs with hemiplegia in 
lesions of the internal capsule, but the eyes can be closed. 
The tongue deviates when protruded toward the paralyzed 
side. Aphasia of some kind may accompany right hemi¬ 
plegia or may occur alone. Hemianaesthesia develops after 



Fig. 51. —The motor tract (Starr): S, fissure of Sylvius ; JVL, lenticular nucleus; OT, 
optic thalamus; JVC. caudate nucleus; C, crus ; P, pons; M, medulla; O, olivary body. 
The tracts for face, arms, and legs gather from the lower, middle, and upper thirds of the 
motor area, pass into the capsule, and through the crus and pons, where the face-fibres cross 
to the opposite VII. N. nucleus, while the others pass on to the lower medulla, where they 
partially decussate to enter the lateral column of the cord, the non-decussating fibres pass¬ 
ing into the ant. median columns. Lesion in cortex causes monoplegia; in capsule, hemi¬ 
plegia; in pons, alternating paralysis. 


lesions of the posterior portion of the internal capsule, but 
is seldom absolute or permanent. Mental symptoms attend 
48 






















754 MANUAL OF THE PRACTICE OF MEDICINE . 

recovery in the majority of cases, and consist of irritability 
of temper, imperfect memory, bewilderment, delirium, or 
even dementia. These mental symptoms may clear away or 
may remain. Crossed facial paralysis occurs with destruc¬ 
tive lesions of the lower portion of the pons (see Fig. 51). 
Small hemorrhages in the cortex cause monoplegia accord¬ 
ing to their situation. Hemianopsia occurs if the lesion in¬ 
volve the optic tracts or the cuneus. 

Prognosis.— Small hemorrhages in the cortex may be 
recovered from without extensive or permanent paralysis. 
If the speech-centre be involved, some degree of aphasia 
may remain. Large central hemorrhages rupturing into 
the ventricles are rapidly fatal. Hemorrhages into the basic 
ganglia and the internal capsule may be fatal. In case of 
recovery from the coma, permanent hemiplegia with con¬ 
tracture is the result. Coma persisting for more than forty- 
eight hours, congestion and oedema of the lungs, low initial 
temperature and high secondary rise with delirium and 
stupor, albuminuria, and the rapid formation of atrophic 
bed-sores are indications of a speedy termination. 

Treatment.— The patient should be kept quiet, with the 
head high. Ice may be applied to the head, and hot bottles 
to the feet. In robust patients with high arterial tension 
venesection should be resorted to \ but this is contra¬ 
indicated if the blood-tension is low and the pulse is weak. 

If the tongue falls back and mucus collects in the throat, 
the patient should be rolled to one or the other side. 
Many patients, according to Bowles, are allowed to suffocate 
from lack of this precautionary procedure. The mouth 
should be cleansed with antiseptic solutions to diminish the 
danger of septic broncho-pneumonia. A laxative should be 
given at the onset— 1 or 2 drops of croton oil or ^ grain of 
elaterium. For throbbing pulse and high tension aconite 
may be given if venesection cannot be performed. 


EMBOLISM OF THE CEREBRAL ARTERIES. 755 

The paralyzed limbs should be massaged to maintain 
their nutrition. Faradism is indicated after the lapse of one 
or two weeks, but when paralysis has lasted for several 
months and late rigidity with contracture has occurred, 
further use of electricity is hopeless. 

EMBOLISM OP THE CEREBRAL ARTERIES. 

Etiology and Synonym. —The usual origin of the em¬ 
bolus is from the valves of the left heart; less frequently 
the embolus arises from aneurysm or atheroma of the aorta 
or the great vessels of the neck, or from the lungs. The 
embolus may be part of a thrombus that has formed in the 
auricular appendix, most commonly associated with the 
puerperal state. Septic emboli occurring during the course 
of ulcerative endocarditis and abscess of the lung give rise 
to cerebral abscesses, and will be considered under that 
heading. Embolism is most frequent in young adults, and 
both sexes are affected in about equal proportions, although, 
according to the statistics of some authors, the condition 
seems more prevalent among women. Synonym : Cerebral 
softening. 

Pathology.—The middle cerebral artery or one of its 
branches is occluded in 90 per cent, of all cases, the left 
artery being more frequently involved than the right. Less 
frequently are involved the basilar, posterior cerebral, ver¬ 
tebral, anterior cerebral, and the internal carotid. As col¬ 
lateral circulation is never sufficient to maintain the nutrition 
of the brain-tissue whose blood-supply is suddenly cut off 
by the occlusion of its nutritive artery, softening and de¬ 
generation ultimately result. The nerve-elements are infil¬ 
trated with serum and undergo fatty degeneration. If the 
affected area be the seat of a reflux of venous blood, it will 
be stained red—“ red softeninglater, when the haemo¬ 
globin becomes altered, “yellow softening” results. If 


756 MANUAL OF THE PRACTICE OF MEDICINE. 

there be no reflux of blood, “ white softening ” results. No 
matter what the color of the softened spot may be, the 
actual disease process is the same in all cases. The soften¬ 
ing process proceeds rapidly and is usually complete in one 
or two days. The area of softening may remain unchanged 
for considerable time, or may be absorbed, leaving a cicatrix 
which may be pigmented. In other cases the softened atea 
is replaced by a cyst with connective-tissue walls. 

The symptoms depend upon the artery occluded. 

I. Embolism of the Middle Cerebral Artery—(a) The onset 
differs from that of hemorrhage in the following particulars : 
(i) There are no premonitory symptoms; (2) the onset is 
more sudden \ (3) coma is less complete and is shorter in du¬ 
ration ; (4) in many cases unconsciousness is not lost, but the 
patient becomes dizzy and bewildered ; (5) convulsive move¬ 
ments of muscles ultimately to be paralyzed occur in one- 
quarter of the cases ; (6) there are no signs of cerebral com¬ 
pression ; vomiting, hard pulsating arteries, slow pulse, 
flushed face, and stertor consequently do not appear; (7) 
the initial temperature changes are slight, but in a few days 
fever may develop. 

(b) Permanent Symptoms .—If the trunk of the middle 
cerebral artery be blocked, hemorrhage and paralysis of the 
face and tongue occur on the side opposite to the lesion. 
There may be aphasia if the left cerebral artery is occluded. 
Attempts at collateral circulation are attended by a decided 
improvement in the patient’s condition in from twelve to 
thirty-six hours. The improvement may continue or may 
be but temporary. The sudden onset of hemiplegia, the tem¬ 
porary improvement, and the relapse are characteristic of 
embolism. The subsequent course resembles that following 
hemorrhage. The mind in embolism, however, is less fre¬ 
quently affected. If the embolus lodges in a small cortical 
artery, the softening will be of a small area, so that mono- 


EMBOLISM OF THE CEREBRAL ARTERIES. 757 


plegia or aphasia alone may develop. In these cases the 
stage of onset may not be well marked. 

The following symptoms follow occlusion of the other 
arteries : 

2. Vertebral Artery. —Symptoms of acute bulbar paralysis 
occur, leading to speedy death. 

3. Basilar Artery. —There is bilateral paralysis with spasm 
and rigidity. Symptoms of acute bulbar paralysis occur, 
and death follows with a high ante-mortem temperature. 

4. Internal Carotid Artery. —Owing to perfect anastomosis, 
no symptoms may result. In other cases a transient or 
permanent hemiplegia may develop. 

5. Anterior Cerebral Artery. —No symptoms may result, 
or there may be mental weakness. 

Diagnosis from cerebral hemorrhage : 


Hemorrhage. 


Embolism. 


Adults between 40 and 80. 
Hypertrophied heart. 
Endarteritis. 

Right middle cerebral usually. 
Aphasia less often. 
Monoplegia rare. 

Prodromal symptoms. 

Coma profound. 

Convulsions rare. 

Cerebral compression. 


Young adults. 

Endocarditis usual. 

Not essential. 

Left middle cerebral. 

Aphasia more often. 

Monoplegia common. 

No prodromal symptoms. 

Coma slight, transient, or absent. 
Convulsions in 25 per cent. 

No cerebral compression. 


The prognosis as regards the attack is, as a rule, some¬ 
what better than in hemorrhage. From the resulting paralysis 
recovery is not usualy, to be expected. 

The treatment resembles that of hemorrhage, except that 
venesection should not be resorted to. Active purgation is 
not necessary, as in hemorrhage. The heart’s action is 
often so weak and irregular as to require the use of stim¬ 
ulants and digitalis. 




758 MANUAL OF THE PRACTICE OF MEDICINE . 


THROMBOSIS OP THE CEREBRAL ARTERIES. 

Etiology.—Thrombi may form in an artery from disease 
of its wall, from embolism, or from pressure on the vessel, 
as from a tumor. Thrombosis may also occur after ligation 

of the internal carotid artery. 

The pathology resembles that of embolism, except that 
the softening occurs more gradually; otherwise the results 
of the two conditions are identical. The middle cerebral 
and basilar arteries are those most commonly affected. 

The symptoms resemble those of embolism, but they 
appear more gradually. There may be premonitory symp¬ 
toms—vertigo, transient aphasia or hemiplegia, and drowsi¬ 
ness. Hemiplegia slowly develops, taking several hours for 
its completion, and the patient gradually becomes comatose. 

The prognosis and treatment are those of embolism. 

ANEURYSM OP THE CEREBRAL ARTERIES. 

Etiology.—The condition occurs in middle age and is 
more frequent in men. The etiology is that of endarteritis 
and aneurysm in general. In many cases aneurysm follows 
embolism, the embolus disappears, and dilatation follows 
the secondary inflammatory changes in the coats of the 
artery. 

Pathology.—The aneurysm occurs most frequently on 
the central, basilar, and internal carotid, less frequently 
upon any of the branches of the circle of Willis. The 
aneurysm is usually small, rarely exceeding the size of a 
cherry, and is usually sacculated. 

The symptoms are those of tumor at the base of the 
brain, and hemorrhage. The pressure-symptoms are those 
of a small basal tumor, the involvement of the cranial nerves 
being especially frequent. Of suspicious significance is the 
occurrence of crossed hemiplegia and third-nerve paralysis. 


ANEURYSM OF THE CEREBRAL ARTERIES. 759 


The accompanying illustration (Fig. 52) shows that only 
pressure on one crus could cause such a distribution of 
paralysis, and the most likely thing to press on the crus is 
an aneurysm at the base of the brain. 



Fig. 52. —Diagram of a section through the crus, etc., in front of the corpora quadrigemina 
(modified from Wernicke) : P C, posterior commissure; Aq., aqueduct of Sylvius; P L, 
posterior longitudinal fibres; III., third nerve; L B, Luy s body; OP 1, optic tract; 
A, aneurysm causing compression-paralysis of third nerve on same side, and opposite 
hemiplegia. 


The symptoms of rupture lead quickly to a fatal issue, 
and the sudden occurrence of a large meningeal hemor¬ 
rhage at the base of the brain is the first information of the 
disease in the majority of cases. 

The prognosis is exceedingly bad. 

Treatment.—If the diagnosis of aneurysm be made, the 
patient is to be put to bed, the circulation is to be rendered 
tranquil, and iodide of potassium is to be given as for aortic 
aneurysm. The vertebral or the internal carotid artery may 
be ligated as an extreme measure, but the results of such 
surgical treatment are not good. 







760 MANUAL OF THE PRACTICE OF MEDICINE. 

THROMBOSIS OF THE VENOUS SINUSES. 

Etiology. —Primary or marantic thrombosis occurs as a 
terminal event in cachectic conditions, and is not infrequent 
in the aged. Infants during the first six months of life may 
be affected, usually after exhausting diarrhceal diseases. 

Secondary thrombosis complicates embolism and cerebral 
tumors producing pressure upon a sinus. I11 these cases 
the clot is not septic. 

Septic thrombus occurs with disease or injury of the 
cranial bones or of the middle ear, with meningitis, and with 
suppurative disease or erysipelas of the scalp, face, or orbit. 

Pathology. —The effect of a clot within a venous sinus 
or a vein is to cause intense congestion and oedema of the 
brain-territory the circulation of which thus becomes ob¬ 
structed. Softening of the brain-tissue may ultimately 
result. Septic thrombi soften, break down, and may give 
rise to embolic abscesses or to purulent meningitis. 

Symptoms. — General cerebral symptoms, which are 
usually present, consist of apathy, stupor, delirium, con¬ 
vulsions, muscular rigidity, vomiting, optic neuritis, and 
coma. Localizing symptoms do not usually occur. The 
cerebral symptoms are most marked when the superior 
longitudinal sinus is involved, but they are never character¬ 
istic. Of diagnostic importance are oedema and distention 
of the veins outside the skull,dn the parts from which the 
veins pass through the bones to join the internal sinuses, as 
in the following instances: Thrombosis of the superior 
longitudinal sinus causes congestion and oedema of the sides 
of the head and forehead, prominence of the anterior fonta- 
nelle in children, and epistaxis. Thrombosis of the caver¬ 
nous sinus causes oedema and congestion of the eyelid and a 
prominence of the eyeball. Thrombosis of the lateral sinus 
causes oedema and congestion over the mastoid. 


CEREBRAL ENDARTERITIS. 


761 


Septic thrombi give rise to septic symptoms—chills, in¬ 
termittent or remittent pyrexia, and the “ typhoid state.” 
The course of the disease may be complicated by menin¬ 
gitis or abscesses of the brain. 

The duration of the disease is from a few days to several 
weeks. 

The prognosis is bad, except that in case of small, non- 
septic thrombi recovery may be possible. 

Treatment. —The shoulders and the head should be 
raised in bed to facilitate the venous outflow of blood. The 
lateral sinus has been explored and septic clots removed, 
with recovery. Otherwise the treatment is symptomatic. 

CEREBRAL ENDARTERITIS. 

Etiology. —Cerebral endarteritis usually occurs in males, 
and is a disease of middle and advanced life. The condi¬ 
tion may be due to senile degeneration of the arteries, 
chronic alcoholism, gout, syphilis, or chronic nephritis. 

The pathology is that of endarteritis (see Arterio-cap- 
illary Fibrosis). The walls of the cerebral arteries are 
thickened and rigid, and may be the seat of atheroma or of 
fatty degeneration. Increased connective tissue in the intima 
may lead to occlusion (“ obliterating endarteritis ”). Such 
degenerated arteries cause an irregularly diminished supply 
of blood to the brain, are subject to spasm, and may lead 
to softening of the brain, to miliary aneurysms and hemor¬ 
rhage, or to larger aneurysms of any of the cerebral arteries. 

Symptoms. —Three groups of clinical symptoms may be 
described: 

1. Symptoms of Brain-ancemia .—The patient suffers from 
headache, dizziness, spots before the eyes, and buzzing 
noises in the ears, and becomes unable to concentrate the 
mind for any length of time. These symptoms are com¬ 
mon to brain-anaemia from any cause. 


762 MANUAL OF THE PRACTICE OF MEDICINE. 

2. Suddenly-induced Ancemia from Spasm. —Spasm may 
occur without known cause at any time, or may follow 
mental excitement or over-eating or drinking. The spasm 
is most common in the middle cerebral artery. In mild 
cases the patient will suddenly develop a partial paralysis 
of the arm or leg, or will become aphasic. Hemianopia 
may occur. The onset is usually accompanied by a “ wave 
of faintness ” and mental bewilderment, but actual loss of 
consciousness does not often occur. Spasm may precede 
the muscular weakness. These attacks are usually tem¬ 
porary, lasting but an hour or so and then wearing off; they 
are liable to be repeated. In other cases the spasm leads to 
softening and the symptoms become permanent. In severe 
cases the patient loses consciousness, although the coma is 
not as complete as in hemorrhage and is of shorter dura¬ 
tion. Hemiplegia with or without aphasia develops, and 
may be preceded by convulsive movements of the muscles. 
The temperature rarely undergoes initial changes, and there 
are no symptoms of compression (slow pulse, stertor, 
flushed face, and throbbing arteries), as in hemorrhage. The 
pulse is usually of high tension, owing to the presence of 
general endarteritis and nephritis. Under favorable circum¬ 
stances the spasm passes off and recovery takes place in a 
few hours or days. 

Illustrative Case. —Male, sixty-five years ; chronic nephri¬ 
tis, general endarteritis. 2 P. m., fell unconscious: right 
hemiplegia, aphasia; pulse 70, of high tension ; no stertor ; 
temperature normal. 12 P. M., conscious; begins to move 
and to talk. 4 A. m., walked and talked; is rational. 6 a. m., 
perfectly recovered. 

3. Symptoms of Brain-softening. —If the spasm be too long 
continued, or should a thrombus form in the vessel, the 
brain-tissue, thus deprived of its blood-supply, will die and 
soften as in embolism or thrombosis. A similar effect is 


CEREBRAL ENDARTERITIS. 


7 6 3 


produced by obliterating endarteritis. In these cases the 
patient does not recover. If the softened area be extensive, 
the patient will die in a few days in coma with hemiplegia, 
death usually being due to pulmonary oedema. In some 
cases coma is not marked at first, so that paralysis without 
loss of consciousness is regarded as indicative of acute soft¬ 
ening from arterial obstruction, however produced. If a 
smaller area be involved, the patient will live, but with per¬ 
manent paralysis or aphasia. In these cases mental de¬ 
rangement is common. 

The diagnosis is made by the presence of extensive 
arterial degeneration, by the history of previous attacks fol¬ 
lowed by recovery, by the absence of symptoms of cerebral 
compression, by the absence of causes for embolism, and by 
the rapid recovery under appropriate treatment. When 
softening occurs the diagnosis from thrombosis cannot be 
made. 

Prognosis. —As the lesion is continuous and progressive, 
there is liability to recurring attacks which tend to become 
more and more severe. The prognosis is rendered worse 
by the nephritis, by the atheroma of the aorta and the 
coronary arteries, and by the chronic alcoholism if such a 
habit exists. The danger of hemorrhage must also be con¬ 
sidered. The immediate prognosis during an attack de¬ 
pends upon the duration of the spasm and upon the chances 
of a thrombus forming in the vessel; a positive assurance 
of recovery, therefore, should never be made. 

Treatment .—Between attacks the treatment should be 
directed toward the arterial degeneration (see Arterio-capil- 
lary Fibrosis). For the anaemic symptoms the arteries may 
be relaxed with small doses of potassium iodide, nitro¬ 
glycerin, or chloral hydrate. Digitalis is contiaindicated. 

At the time of spasm the arterial dilators above mentioned 
should be pushed to physiological limits. The bowels 


764 MANUAL OF THE PRACTICE OF MEDICINE. 


should be moved, and the functions of the skin and kidney 
should be stimulated, to eliminate from the system such 
noxious products as might cause arterial spasm. 

When actual softening occurs treatment becomes inopera¬ 
tive. 


3. DISEASES OF THE BRAIN-SUBSTANCE. 

CEREBRAL LOCALIZATION. 

Cortical Areas. — 1. The motor area is located in the 
cortex of the anterior and posterior central convolutions 
bordering upon the fissure of Rolando. The area of each 
hemisphere controls muscular movements of the opposite 
side of the body. The different groups of muscles are 



Fig. 53.—The functional areas of the brain, left hemisphere (Starr). 


supplied by definite portions of the motor area, as is shown 
by the accompanying diagram (Fig. 53). Irritation of the 
motor area gives rise to localized spasm or convulsions 
(“ Jacksonian epilepsy ”). Destructive lesions cause paral¬ 
ysis. Slowly spreading lesions, as the growth of a tumor, 









CEREBRAL LOCALIZATION. 765 

cause spreading irritation followed by destructive symptoms 
(convulsions followed by paralysis), and involve fresh 
groups of muscles, so that the size and position of the 
lesion may be determined accurately. Cortical paralysis is 
monoplegic and is associated with increased reflexes, but 
the paralyzed muscles do not atrophy and the electrical 
reactions are unchanged. Destructive lesions in the motor 
tract from the cortex to the anterior nerve-cells in the spinal 
cord are regularly followed by descending degeneration (see 
Secondary Lateral Sclerosis). 

2. The sensory area is in the cortex posterior to the motor 
area, but accuracy in localization cannot be obtained. The 
tactile sensibility of muscles seems to be in the motor area. 



Fig. 54. —Inner surface of right hemisphere : A, ascending frontal. B, ascending parietal 
convolution; c, terminal portion of the sulcus centralis, or fissure of Rolando; CC, corpus 
callosum, longitudinally divided ; Cf, collateral or occipito-temporal fissure (Ecker); cm, 
sulcus calloso-marginalis ; D, gyrus descendens ; F\, median aspect of the first frontal con¬ 
volution ; G/, gyrus fornicatus ; H, gyrus hippocampi; A, sulcus hippocampi, or dentate 
fissure; O, sulcus occipitalis transversus ; oc, calcarine fissure; oc', superior, oc", inferior 
ramus of the same; Oz, cuneus ; /<?, parieto-occipital fissure; Pi", precuneus ; J\, gyrus 
occipito-temporalis lateralis (lobulus fusiformis); 7$, gyrus occipito-temporalis medialis 
(lobulus lingualis) ; U, uncinate gyrus. 

3. The visual area is in the occipital lobe, including the 
cuneus on the median surface and the occipital convolutions 
on the convexity (see Fig. 54). Each area receives impres- 




y 66 MANUAL OF THE PRACTICE OF MEDICINE. 

sions from the same side of each retina, so that distinctive 
lesions cause failure of visual perception in the same side 
of each retina, the blind field of vision being therefore on the 
opposite side to the lesion (“ homonymous hemianopsiasee 
Fig. 55). Irritation of the visual area causes visual halluci¬ 
nations. Destruction of the visual area of the left side is 
followed by word-blindness. 

4. The auditory area is in the first and second temporal 
convolutions. Deafness from unilateral lesions is seldom 
noticeable. Lesions of the auditory centre on the left side 
are followed by auditory amnesia, or word-deafness. 

5. The smell- and taste-centres are found at the tip of the 
temporal lobe, where it rests upon the sphenoid bone. Uni¬ 
lateral lesions do not produce noticeable symptoms. 

6. The speech-centres are found in the left hemisphere in 
right-handed people, in the right hemisphere in those who 
are left-handed. Reflex and automatic speech may receive 
impulses from both hemispheres. There are four speech- 
centres : 

(a) The motor speech-centre is in the posterior portion of 
the third left frontal convolution, and governs the motions 
concerned in talking. Destructive lesions produce loss of 
the memory of the effort needed to pronounce a word (“ mo¬ 
tor aphasia”). Such patients cannot talk or read aloud,but 
understand what is said to them, and may be able to write. 

(b) The auditory speech-centre is in the first and second 
left temporal convolutions, and controls the understanding 
of language and the recollection of the names of things. 
When the centre is destroyed “ word-deafness ” results. 

(c) The visual speech-centre is in the cuneus and the 
occipital convolutions. When destroyed “ word-blindness ” 
results, the patient being unable to understand written lan¬ 
guage. 

{d) The writing speech-centre is supposed to be within 


CEREBRAL LOCALIZATION. 


767 



Fig. 55.—The visual tract (Starr): the result of a lesion anywhere between the chiasm 
and the cuneus is to produce homonymous hemianopsia. H, lesion at chiasm causing 
bilateral temporal hemianopsia ; N, lesion at chiasm causing unilateral nasal hemianopsia ; 
T, lesion at chiasm causing unilateral temporal hemianopsia; SN, substantia nigra of crus ; 
L, lemniscus in. crus; RN, red nucleus; III., third nwves, 























;68 MANUAL OF THE PRACTICE OF MEDICINE. 


the motor speech-centre. If the patient be unable to write, 

the condition is termed “ agraphia.” 

Lesions destroying commissural or association fibres be¬ 
tween the various speech-centres cause displacement of 
words, so that the patient may talk jargon. To this con¬ 
dition the terms “ mixed aphasia ” and “ paraphasia ” have 


been applied. , , 

7. The intellectual area is located in the frontal lobes, but 


no localizing symptoms occui 

Subcortical Localization 



Fig. 56.—The sensory tract in the 
crus, pons, and medulla, showing nu¬ 
cleus and roots of V. nerve (Starr): A, 
lesion causes hemianaesthesia ; B, lesion 
causes alternating hemianaesthesia left 
face and right side of body. 


— Centrum Ovale .—Lesions 



paralysis—left facial, right extremities ; C, 
lesion causes paralysis of limbs and tongue ; 
D, lesion causes paralysis of limbs of oppo¬ 
site side; E , lesion in motor decussation 
causes bilateral paralysis. 


cause paralysis, which are hemiplegic the nearer the lesion 
is to the internal capsule, monoplegic the nearer to the cortex. 








ABSCESS OF THE BRAIN. 769 

Hemianaesthesia results from lesions in the posterior por¬ 
tion, and hemianopsia may also result. 

Internal Capsule. —Lesions of the anterior two-thirds 
cause opposite hemiplegia, with involvement of the tongue 
and face and with descending degenerations (see Fig. 51). 
The power to wink is maintained. Lesions of the posterior 
third cause hemianaesthesia. 

Lesions of the lower portion of the pons cause crossed 
facial paralysis (see Fig. 57). The facial paralysis resembles 
the cerebral form in that the lower fibres alone are involved. 

If the nucleus of the facial nerve be involved, the patient 
will not be able to wink, and atrophy and the reaction of 
degeneration will be developed. Lesions in the lower por¬ 
tion of the pons may also cause alternating hemianaesthesia 
(see Fig. 56). 

Basic Ganglia .—Destructive lesions cannot be diagnosed 
from those of the tracts which lie near them. 

Corpora Quadrigemina. —Destructive lesions cause stag¬ 
gering gait, blindness, nystagmus, and ophthalmoplegia. 

Cerebellum .—Lesions cause staggering gait, but the ataxia 
disappears when the patient lies down. Vertigo is marked. 
Irritation of the middle peduncle causes staggering toward 
the side of the lesion; destruction of the middle peduncle 
causes staggering away from the side of the lesion. 

ABSCESS OF THE BRAIN (SUPPURATIVE 

ENCEPHALITIS). 

Etiology. —Infection of the brain-substance may occur 
through the following channels : 

1. By Continuity through the Cranial Bones .—Thus abscess 
arises from injury of the scalp or skull (35 per cent.), from 
caries of the cranial bones (10 per cent.), from diseases of 
the middle ear (40 per cent.), or from chronic suppurative 
49 


770 MANUAL OF THE PRACTICE OF MEDICINE. 

rhinitis (io per cent.). In these cases the abscess is often 
associated with meningitis. 

2. Through the Blood-vessels .—Septic emboli may occur 
during the course of pyaemia, malignant endocarditis, gan¬ 
grene, or suppuration of the lung or of the pleura. Abscess 
of the brain may be a sequel of epidemic influenza. 

Abscess of the brain usually occurs between the twentieth 
and fortieth years, and is more common in men than in 
women. 

Pathology. —Abscess is most common in the temporo- 
sphenoidal lobe. One-eighth of the cases occur in the cere¬ 
bellum and are usually secondary to mastoid disease. The 
abscess at first is limited by jagged and necrotic brain-tissue 
infiltrated by pus-cells, or, in time, a fibrous capsule may be 
formed. Rupture into the ventricles may result; rupture 
through the cortex induces a peracute meningitis. The 
cerebral sinuses may be the seat of infective thrombi. Em¬ 
bolic abscesses are usually multiple. Abscess of the brain 
may run an acute or a chronic course. 

The symptoms of acute cases may be divided into three 
groups: 

1. Symptoms of Pressure .—Headache is severe and con¬ 
stant, persists during sleep and stupor, and may be localized. 
Vomiting is frequent and is not induced by eating. Optic 
neuritis commonly develops. The pupils are apt to be ir¬ 
regular. The pulse is apt to be slow, running from 60 to 
70. Drowsiness alternates with restlessness and delirium, 
and finally merges into coma. 

2. Toxic symptoms are those of an internal abscess. A 
chill occurs at the onset; chills may be repeated at irregular 
periods throughout the disease. Irregular fever occurs, but 
usually there are periods during which the temperature is 
normal or subnormal. The patient finally passes into the 
typhoid condition. 


ABSCESS OB THE BRAIN. 


7/1 

3. Localizing symptoms depend upon the location of the 
abscess, and whether certain portions of the brain are irri¬ 
tated or destroyed. There may be convulsions (general and 
epileptiform, or localized in certain groups of muscles), 
paralyses (either hemiplegic or monoplegic), or aphasia. If 
phlebitis be present, there will be oedema behind the ear and 
a sense of fulness over the jugular vein. If meningitis be 
present, there will be rigidity of the neck and cranial-nerve 
paralysis. 

Abscesses in the frontal lobe may cause only a mental 
dulness. They are usually caused by disease of the nose 
or of the ethmoidal cells. 

In the temporo-sphenoidal lobe there may be no localizing 
symptoms. Abscess of the parieto-occipital region may cause 
hemianopia. 

Cerebellar abscess is usually accompanied by vomiting, 
vertigo, and staggering gait. 

A chronic abscess may develop in some portion of the 
brain that is not highly specialized (“silent region”), become 
encapsulated, and lead to no particular symptoms. After 
the lapse of a number of months, however, it is usual for 
the abscess to show itself by sudden coma or an epileptic 
seizure. These terminal phenomena are due to rupture 
either into a ventricle or through the cortex. 

The diagnosis is based upon the presence of a cause by 
which infection is possible, upon septic symptoms, and upon 
the symptoms of a localized destructive lesion. 

Prognosis.— Acute abscesses terminate in from three to 
fourteen days, rarely extending over thirty days. Chronic 
abscesses may have a latent period of weeks or months, but 
death usually takes place within one or two days of the 
rupture. The prognosis is fatal unless the pus can be 
evacuated. 

Treatment is exclusively surgical, and consists of tre- 


772 MANUAL OF THE PRACTICE OF MEDICINE. 

phining and draining the abscess-cavity. The percentage 
of cases recovering after such operation is increasing year 
by year. 

TUMORS OF THE BRAIN. 

The following are the more frequent varieties of brain- 
tumors encountered: 

1. Tubercle .—Tubercular tumors are usually multiple, 
and are generally found in the cerebellum. 1 hey may grow 
to one or two inches in diameter. One-half of the tumors 
in children are of tubercular origin. 

2. Glioma is a form of tumor peculiar to the nervous 
system, and consists of a fibrillary network and branching 
cells. A variety called “neuro-glioma” contains large 
spindle-cells with single nuclei, and others resembling the 
large ganglion-cells. Gliomata may be hard and may 
resemble an area of sclerosis, or they may be soft and 
highly vascular. Glioma is never sharply defined, but 
fades imperceptibly into the surrounding bone-tissue, hence 
its invasive tendency. Glioma and sarcoma are often com¬ 
bined. 

3. Syphilitic tumors, or gummata,axo. most common in the 
hemispheres and pons, and usually develop from the pia 
mater or the arteries. Gummata are rarely of large size 
and are usually multiple. 

4. Sarcoma usually develops from the membranes or the 
cranial bones, and may reach large size. Myxo-sarcomata 
are not uncommon. 

4. Cancer is almost regularly of secondary growth, and 
may be multiple. Sarcoma or carcinoma starting from the 
membranes may invade the bones and appear externally, 
forming the “ fungus haematodes,” or “ perforating tumor 
of the dura.” 

6. Cysts may be found, resulting from previous hemor- 


TUMORS OF THE BRAIN. 


773 


rhage or from defective development. Hydatid cysts are 
not uncommon in certain countries, as Iceland and Australia. 

Psammoma , cholesteatoma , lipoma , and angioma are rare 
forms of tumor. An aneurysm of one of the cerebral arteries 
forms a tumor which has elsewhere been discussed. 

Pathology.— Except for tubercular and gliomatous 
tumors, the new growth usually starts in the membranes. 
According to Starr, the cerebral cortex is involved in 25 
per cent., the cerebellum in 25 per cent., the centrum ovale 
in 5 per cent., the basic ganglia, the pons, the crus, and 
the corpora quadragemina, each in 10 per cent., other parts 
in 5 per cent., of all cases. The brain-tissue in the neigh¬ 
borhood of a tumor may be hyperaemic and inflamed, or it 
may undergo softening. A localized chronic meningitis 
results if the growth involve the pia mater. If the venous 
sinuses be compressed, the blood may be dammed back, 
and serous effusion may take place within the cavity of 
the ventricles. 

Men are more frequently affected than women, in the 
proportion of 2 : 1. In children, tumors are apt to be 
tubercular; in early life, gummata or gliomata; in middle 
life, sarcomata, gummata, or gliomata; in late life, sarco¬ 
mata, gummata, or carcinomata. Tumors of the brain are 
rare after the age of sixty. 

The symptoms of brain-tumors may be divided into two 
groups: (1) Those due to brain-compression, no matter 
where the growth may be; (2) the localizing symptoms, 
due to localized irritation and destruction of a certain por¬ 
tion of the brain. 

1. General symptoms of brain-compression are tolerably 
constant in all cases of brain-tumor. 

(a) Headache occurs in 95 per cent, of all cases. It is 
usually dull and “ stupefying,” with paroxysmal exacerba¬ 
tions, and it may be general, or localized over the growth, 


774 MANUAL OF THE PRACTICE OF MEDICINE. 

especially in the case of cerebellar tumors. There may be 
localized tenderness over the scalp. The headache differs 
from that of functional origin in that the patient gives 
evidence of pain during sleep or during periods of stupor. 
The headache of brain-tumor is more severe and persistent 
than that of any other disease. 

( b ) Mental disturbances occur in 85 per cent, of all cases. 
The patient becomes dull, apathetic, and inattentive. 
Memory and reasoning are impaired; childishness and 
even dementia or insanity may develop. The characteristic 
speech is an articulation in which the syllables are run to¬ 
gether. In many cases there are morbid erotic desires. 

( c ) Optic neuritis occurs in 80 per cent, of all cases, and 
is usually bilateral. The old name of “ choked disk ” given 
to this condition is inappropriate, as the condition is due, not 
to pressure, but to a descending neuritis. Double optic 
neuritis occurs with lead-encephalopathy, meningitis, cerebral 
abscess, anaemia, and Bright’s disease, but an intracranial 
tumor is by far its most frequent cause. In the first stage 
the disk is swollen, its edges are blurred and striated, and 
the physiological cupping disappears. During the first 
stage there may be no disturbances of vision, but dimness 
of vision, restricted field of vision, or color-blindness may 
be noticed. Atrophy of the optic nerve usually supervenes ; 
the disk has a glassy, white appearance, and the arteries 
are small. In the stages of atrophy impairment of vision, 
or even total blindness, may result. Optic neuritis, while 
not a localizing symptom, is most frequent with tumors of 
the cerebellum and of the basic ganglia. 

( d) Vomiting occurs in 50 per cent, of the cases, and is 
most marked with cerebellar tumor. The vomiting is 
“ purposeless,” has no relation to meals or to local causes, 
and may assume a projectile character. 

(e) Vertigo is present in 20 per cent, of the cases, and is 


TUMORS OF THE BRAIN. 775 

most constant and severe with tumors of the cerebellum. 
In many cases vertigo persists while the patient is lying 
down, so that he will hold on to the side of the bed in 
order “ not to be thrown out.” In other cases vertigo is 
noticed only with a change in position. 

(f) General epileptiform convulsions may occur, and 
glycosuria and polyuria have been noticed, especially with 
cerebellar tumors. 

(g) The pulse is usually slower, varying between 50 and 
70. The boivels are usually constipated. 

2. Localizing Symptoms. — (a) Tumors of the frontal lobes 
give rise to mental dulness, irritability, and dementia. 
There may be loss of smell. The motor area may finally 
be encroached upon. 

( b ) Tumors of the motor area give rise at first to mono¬ 
spasm (“ Jacksonian epilepsy ’’), preceded by sensory aurae. 
As the tumor grows the spasms become more diffused, so 
that by considering the “ signal symptom ” and the march 
of the spasm the exact location and rapidity of growth may 
accurately be determined. Monoplegia succeeds mono¬ 
spasm, the lesion, at first irritative, later becoming destruc¬ 
tive. Lesions extending deeply toward the capsule may 
cause hemispasm and hemiplegia. The paralyzed muscles 
may, to a moderate degree, be insensitive to pain, touch, 
and temperature. 

(, c ) Tumors of the parieto-occipital lobe may give rise to 
no localizing symptoms. Word-blindness results from 
lesions of the left angular gyrus. 

(d) Tumors of the occipital lobe produce hemianopia, 
and, if the left hemisphere be involved, there may result 
word-blindness and mind-blindness. The latter symptom, 
also known as “ soul-blindness,” consists in the incapacity 
to understand the nature of things which one sees. Bi¬ 
lateral lesions may produce blindness. 


776 MANUAL OF THE PRACTICE OF MEDICINE. 

(V) Tumors of the temporal lobe on the left side may 
cause word-deafness. By extension the motor area may be 
involved. 

(/) Tumors of the basic ganglia give rise to no character¬ 
istic symptoms unless the internal capsule is involved or 
the lateral ventricles become distended by pressure. 

(g) Tumors of the corpora quadrigemina produce inco¬ 
ordination, forced movements, and oculo-motor paralysis. 

( h ) Tumors of the crus cause opposite hemiplegia or 
hemianaesthesia, with paralysis of the third nerve on the 
same side as the lesion. 

(i) Tumors of the pons are chiefly productive of paralysis 
of the nerves emerging from this region on the same side 
as the lesion, with opposite hemiplegia or hemianaesthesia. 
Conjugate deviation of the eyes away from the side of the 
lesion may be observed. 

(j) Tumors of the medulla may cause paralysis of the 
cranial nerves alone, with the symptoms of bulbar paralysis ; 
or there may be hemiplegia or convulsions. 

( k ) Tumors of the cerebellum present distinct peculiarities, 
especially if the middle lobe be involved. The symptoms 
consist of marked occipital headache from pressure of the 
tentorium ; marked vertigo, especially if the middle lobe be 
implicated; cerebellar ataxia, and a pitching or reeling gait. 
Involvement of the middle lobe causes pitching toward the 
side of the lesion, forward or backward according to whether 
the anterior or pdsterior portion of the lobe be involved. 
Optic neuritis and vomiting occur early and are marked. 
The pressure of the growth on the straight sinus causes ve¬ 
nous congestion and distention of the ventricles with serum 
(see Fig. 58). In this way mental slowness and general 
convulsions may be developed. Pressure of the growth on 
the medulla may cause bilateral rigidity, increased reflexes, 
and vaso-motor symptoms in different parts of the body. 


TUMORS OF THE BRAIN. 


777 


The diagnosis of brain-tumor may be made from the 
general symptoms alone. Strict localization is often pos¬ 
sible. 

The duration varies from one to three years. In rare 
cases the symptoms may persist for a longer time than this. 

The prognosis is bad, except for gumma and operable 
growths. 



p IG _Diagram showing the manner in which compression of the veins of Galen is 

produced by a tumor of the cerebellum, more especially of its middle lobe (after Stephen 
Mackenzie). The letter a points to the superior and b to the inferior longitudinal sinus, 
c to the straight sinus, d to a tumor beneath the tentorium, and eto the veins of Galen. 


Treatment.—The patient should be given mercurial in¬ 
unctions, and potassium iodide up to 300 grains daily. 
If the growth be gumma, the results are often brilliant. In 
tubercular tumors a general tonic treatment is indicated, as 
there are cases reported in which the tubercular tumors 
have undergone encapsulation and calcific change, and 
have ceased developing. 

The surgical treatment consists in trephining and remov¬ 
ing the tumor. Brilliant results have followed this pro¬ 
cedure in cases in which the tumor was superficial, accessi¬ 
ble, and capable of enucleation. The actual number, how- 









778 MANUAL OF THE PRACTICE OF MEDICINE. 


ever, of operable cases is small (less than 5 per cent., 
according to Dana). In case of doubt an exploratory 
trephining is advisable. 

CEREBRAL ATROPHY IN CHILDREN. 

Etiology. —Cerebral atrophy in children may be congen¬ 
ital, or may be acquired by injuries at birth or by such dis¬ 
eases as occur in adults. In 343 cases collated by Starr, 
the following primary lesions have been followed by atro¬ 
phy of the brain in children : 

Porencephalus , a localized atrophy in the cerebral hemi¬ 
sphere, which may be deep enough to open into a ventricle 
—132 cases. 

Sclerotic atrophy , atrophy of nerve-elements with increase 
of connective tissue, involving one or both hemispheres, or 
part of a hemisphere, or in small scattered areas—97 cases. 

Maldevelopment —32 cases. 

Atrophy following softening produced by embolism or 
thrombosis, and limited to arterial districts of the brain— 
23 cases. 

Meningo-enccphalitis , shown by thickening and adhesion 
between the pia and the brain, with atrophy of the cortex— 
21 cases. 

Cysts lying on the brain, causing atrophy by pressure, or 
associated with atrophy due to the original disease of which 
the cyst remains as a trace—14 cases. 

Hemorrhage on or in the brain—18 cases. 

Hydrocephalus with thinning of the brain-tissue—5 cases. 

Unilateral hydrocephalus —1 case. 

An inflammation of the cells of the motor cortex anal¬ 
ogous to anterior poliomyelitis has been described by Strum- 
pell, but lacks positive evidence. 

Symptoms. —Four clinical groups may be described : 

1. Infantile Hemiplegia. —The attacks are usually pre- 


CEREBRAL ATROPHY IN CHILDREN. 


779 


ceded by convulsions and fever followed by unconscious¬ 
ness and hemiplegia. A gradual improvement occurs 
up to a certain point, after which the symptoms remain 
permanently. The paralysis may be evident, or there 
may only be stiffness and clumsiness in performing volun¬ 
tary motions. There may or may not be aphasia. The 
paretic muscles show lack of development and are small 
and cold. Rigidity is due to a condition of exaggerated 
reflexes. The electrical reactions are unchanged. Essential 
atrophy of the muscles does not occur. The affected muscles 
may show tremor or inco-ordinate choreiform movements 
(“post-hemiplegic chorea”), or there may be involuntary 
rhythmical spasms of the fingers and the toes (“ athetosis ”). 
Various deformities, such as club-foot, arise from the action 
of the unparalyzed muscular antagonists. Epileptiform 
attacks occur in one-half the cases. The patient is apt to 
be imbecile or feeble-minded. 

Infantile hemiplegia dating from birth is to be ascribed to 
meningeal hemorrhage occurring from traumatism during 
a difficult labor. 

2. A double hemiplegia due to meningeal hemorrhage 
during birth is described as spastic diplegia or birth- 
palsy. More rarely the condition follows fevers or convul¬ 
sions. The extremities are paretic and rigid from over¬ 
reflexes. The mental condition is defective, and convul¬ 
sions are common. The muscles act irregularly (“ chorea 
spastica ”), or there may be bilateral athetosis. 

3. In some patients mental defects constitute the principal 
symptoms. In these cases the sclerotic atrophy involves 
the anterior portion of the brain. The following descrip¬ 
tion is given by Starr: 

“The child may be slow in learning to talk; may seem 
unable to fix its attention upon anything continuously; may 
be exceedingly active, in constant motion—the activity be- 


780 MANUAL OF THE PRACTICE OF MEDICINE. 

ing, however, aimless; may throw things about, or tear 
things up, or put everything into its mouth; may be very 
difficult to manage because of its inability to retain and 
combine impressions with sufficient power to reason upon 
them; and may therefore be incapable of appreciating the 
meaning of punishment, if this be inflicted. Such children 
may have good powers of perception, may recognize per¬ 
sons and objects, show pleasure at bright colors or music 
or caresses, but fail to show evidence of thought in the 
sense of reasoning power, judgment, or self-control. Some 
patients constantly drool at the mouth, cannot be taught 
cleanly habits, and are manifestly imbecile. Other patients 
are quite bright in many directions, may even be precocious, 
show talents in music or drawing, or fondness for mathe¬ 
matics, designing, or languages, yet are apparently unable 
to appreciate moral ideas, cannot be taught to tell the truth, 
are cruel and bad, will not control any of their impulses, 
and so are the distress and despair of parents and teachers. 
It is those mental qualities which are the product of the 
highest evolution that have failed to develop in this class 
of cases. The final result is that they have to be taken care 
of all their lives, either at home or by attendants, being in¬ 
capable of supporting themselves or directing their conduct. 
Many of them have epilepsy.” 

4. In a fourth set of cases there are neither moral nor 
motor defects, but the patients are subject to epilepsy, and 
they present defects of sensory perception. Many cases of 
deaf-mutism belong to this class. In these patients the 
atrophy affects the temporal and occipital convolutions. 

The prognosis is bad for recovery, although life may not 
be shortened. 

Treatment.—Prophylactic treatment consists in cutting 
short all convulsive seizures in children—by purgatives, hot 
baths, bromides, chloral, or whiffs of chloroform. 


CEREBROSPINAL SCLEROSIS. 781 

When paralysis occurs, the nutrition of the muscles is to 
be maintained by massage and passive motion, and deformi¬ 
ties are to be corrected by surgical or mechanical measures, 
bor the epileptic attacks bromides may be found useful. In 
certain cases of arrested brain-development due to micro- 
cephalic skull the result of premature union of the sutures, 
craniectomy may be resorted to. When clots, cysts, or 
tumors are removable by surgical measures, the chance of 
recovery is increased. Epileptiform convulsions may in some 
cases be reduced in severity and in frequency by removing a 
portion of the skull, so that an increase in the intracranial 
pressure can occur without producing pressure on the brain. 

CEREBRO-SPINAL SCLEROSIS. 

Etiolog-y and Synonyms.—The etiology of cerebro¬ 
spinal sclerosis is obscure. Heredity is marked in a small 
number of cases. The disease may follow any of the infec¬ 
tious diseases, especially scarlet fever. It is most common 
in middle life, but it is not infrequently seen in children. 
Synonyms: Insular, Multiple, or Disseminated sclerosis. 

Pathology.—Throughout the brain and cord are small 
grayish nodules of connective tissue which destroy the 
medullary sheath of the nerves, but leave the axis-cylinder 
unchanged. The cortex is not usually involved. Sclerosis 
of the spinal cord alone is of great rarity. 

Symptoms.—The onset is insidious and is marked by 
feebleness and stiffness of the legs and the arms and by in¬ 
creased reflexes. The feebleness may ultimately develop 
into paralysis, so that the patient becomes bedridden. 
Marked tremor is developed on motion, but ceases when the 
muscles are at rest. The speech becomes scanning and 
“ syllabic.” Rapid oscillation of the eyeballs (nystagmus) 
is usually pronounced. The association of volition-tremor 
with scanning speech and nystagmus forms a characteristic 


yS2 MANUAL OF THE PRACTICE OF MEDICINE. 

symptom-group. The mental state usually becomes pro¬ 
gressively enfeebled. Optic neuritis may develop. Sensa¬ 
tion is usually unaffected, but there may be lightning pains 
and anaesthetic areas as in locomotor ataxia. Vertigo is 
common. There may be apoplectic seizures, with coma, 
fever, and transient hemiplegia, or there may be epileptiform 
convulsions. The patient finally becomes unable to per¬ 
form the ordinary duties of life, by reason of mental weak¬ 
ness, volitional tremor, and muscular feebleness. The course 
of the disease is chronic, with periods of temporary improve¬ 
ment. 

Diagnosis.—The disease may resemble hysteria or Fried¬ 
reich’s ataxia in children. Anomalous cases are occasionally 
encountered, which resemble transverse myelitis, locomotor 
ataxia, or general paresis. 

The prognosis for recovery is bad. 

Treatment is practically unavailing. A course of mer¬ 
cury bichloride with potassium iodide may be tried in alter¬ 
nation with small doses (gr. -^ ) of nitrate of silver. In all 
cases a quiet life is to be advised. 

GENERAL PARESIS. 

Etiology and Synonyms.—The disease is common be¬ 
tween the ages of thirty and fifty-five, and is more frequent 
in men than in women. Heredity appears in 15 per cent, of 
the cases. The exciting cause may be prolonged mental 
strain, excesses, syphilis, alcoholism, and lead-poisoning. 
The disease is not uncommon among active, ambitious 
business-men. Synonyms: Paretic dementia ; General paral¬ 
ysis of the insane ; Chronic meningo-encephalitis ; Chronic 
periencephalitis. 

Pathology.—The membranes are thickened, opaque, and 
adherent in places to the brain-substance ; the cortex is firm 
and more or less atrophied; there is an increase in the 


GENERAL PARESIS. 


783 


cerebro-spinal fluid. Microscopic examination shows an 
increase of connective tissue, with a degeneration and dis¬ 
appearance of nerve-fibres and ganglionic cells. In the cord 
similar sclerotic areas are found in the posterior and lateral 
columns. The ventricles are usually dilated. There may 
be small areas of softening in the brain-substance, associated 
with arterial sclerosis. 

The symptoms begin insidiously with a change in the 
moral nature. The patient becomes inattentive and forget¬ 
ful, and may violate the ordinary rules of decency and 
deportment. There is increasing mental weakness, with 
irritability of temper. A peculiar egotism usually but not 
invariably develops, with delusions of grandeur, so that the 
patient becomes absurdly boastful, and believes himself to 
be possessed of millions of money, or to have made the 
most wonderful inventions, or to be king, emperor, or even 
God himself. Vaso-motor phenomena and general neuras¬ 
thenia add their symptoms. In the earlier stages motor 
symptoms may be noticed : the tongue trembles when it is 
protruded ; the gait is unsteady and shuffling. The pupils 
are frequently unequal. They may react to distance, but 
not to light (“ Argyll-Robertson pupil ”). There may be 
epileptiform seizures or Jacksonian epilepsy, frequently fol¬ 
lowed by transient paralyses. The speech becomes thick, 
owing to the difficulty of pronouncing the lingual and 
labial consonants. Scanning or a slow, hesitating, monoto¬ 
nous speech is common, words and syllables are frequently 
omitted, and the patient stumbles over words. Writing 
becomes uncertain and irregular, and letters or words may 
be omitted; finally the writing becomes totally illegible. 
The gait becomes increasingly impaired, and may be spastic 
or ataxic. The knee-jerk is usually increased. Maniacal 
outbursts may follow the delusions of grandeur, or there 
may be periods of melancholia or of depression. In the 


784 MANUAL OF THE PRACTICE OF MEDICINE . 

last stages the patient becomes demented, the bladder and 
rectum become unretentive, the health fails, and the patient 
becomes bedridden. Death results from exhaustion or from 
intercurrent disease. 

The course of the disease is progressive, with periods of 
temporary improvement. The average duration is from 

three to four years. 

The prognosis is unfavorable. 

Treatment.—In syphilitic cases a thorough course of 
iodide and mercurials should be employed, but not much is 
to be expected from the treatment. Nursing and a quiet 
life in an asylum really constitute the only treatment of the 
disease. 


CHRONIC HYDROCEPHALUS. 

An increase in the amount of fluid in the ventricles 
occurs in a congenital and an acquired form. 

Congenital Hydrocephalus. —No known cause has 
been discovered for this condition. It has occurred in 
several members of the same family. The lateral ventricles 
are principally affected, and are distended with fluid, so that 
the cerebral cortex over them is thin and stretched and 
may be converted to a thin shell less than a quarter of an 
inch in thickness. The sutures and fontanelles are widely 
distended, so that the skull becomes enormously enlarged, 
in some cases exceeding thirty to thirty-two inches in 
diameter for a child of two or three years. The bones of 
the cranium are thinned, the orbital plates are so depressed 
as to cause exophthalmos. The fluid is limpid, contains 
traces of albumin and salts, and sometimes contains urea. 

Symptoms.—The head may be so large at birth as to 
interfere with natural labor. In other cases the head does 
not increase in size until several weeks after birth. The 
child is restless and irritable. There is difficulty in getting 


SYPHILIS OF THE BRAIN. 


78 5 


the child to walk, or the legs may be feeble and in a con¬ 
dition of exaggerated reflexes. A few children are bright, 
but in the great majority some grade of imbecility is 
piesent. Strabismus and optic atrophy may develop; nys¬ 
tagmus is commonly present. Vomiting, coma, and con¬ 
vulsions ultimately appear, and the child rarely lives for 
more than three or four years. 

Acquired Chronic Hydrocephalus. — This condition 
may result fiom compression or obliteration of the straight 
sinus 01 of the passage from the third to the fourth ventricle 
by a tumor; other cases follow meningitis. In a few in¬ 
stances the condition arises without known cause serous 
apoplexy ”). 

The symptoms are obscure, and a diagnosis during life 
is but seldom made. Headache, optic neuritis proceeding 
to atrophy, and attacks of stupor are commonly observed. 
The head in the acquired form does not enlarge. There 
are no localizing symptoms. 

Treatment of Hydrocephalus.—Gradual compression 
of the skull should be made by straps of adhesive plaster 
crossed in various ways. When pressure-symptoms are 
present, puncture of the ventricles by a fine aspirating 
needle and the withdrawal of small quantities of fluid from 
time to time are justifiable procedures. The subarachnoid 
sac between the third and fourth lumbar vertebrae may be 
punctured without risk of injury to the cord, and the fluid 
slowly removed without much danger of collapse. Med¬ 
icines are useless, although inunctions of mercury and the 
administration of potassium iodide have been recommended. 

SYPHILIS OP THE BRAIN. 

Congenital syphilis of the brain may develop during 
early childhood, but it is rare. The acquired form is 
usually a late tertiary manifestation of the disease, although 

50 




736 MANUAL OF THE PRACTICE OF MEDICINE. 

it may develop in from six months to thirty years after the 
primary sore. The earlier occurrence of symptoms is by 
some authors attributed to the appearance upon the mem¬ 
branes of an actual syphilitic eruption analogous to the 
cutaneous exanthems of the secondary period. 

1. Syphilis of the Bones of the Cranium. —The lesion con¬ 
sists in the formation of spots of dry caries, nodes, and 
necrosis. Cerebral symptoms arise only if the membranes 
be secondarily inflamed. If the lesions involve the foramina 
through which the cranial nerves pass, there will be 
developed neuralgic pains or motor spasms, followed by 
anaesthesia or paralysis. 

2. Syphilitic Meningitis. — The membranes show the 
lesions of an acute or chronic inflammation, and are invaded 
by gummata. The symptoms are those of the meningitis 
and those of the multiple tumors pressing on the cortex, 
and according to the predominance of either group of 
symptoms the case will resemble acute or chronic menin¬ 
gitis or cortical tumors. The suggestive points of syphilitic 
meningitis are—(i) Headache, existing several weeks before 
the onset of other symptoms, severe in character, and worse 
at night, preventing sleep; (2) the admixture of symptoms 
of inflammation of the meninges and of cortical tumors ; (3) 
the rapid improvement under treatment. 

3. Gummata of the Brain. —The symptoms of brain- 
tumor are frequently preceded by intense nocturnal head¬ 
ache, by temporary incomplete paralysis of an arm or a leg, 
or by temporary squint. These partial passing palsies are 
quite suggestive of cerebral syphilis. The general and 
localizing symptoms of cerebral gummata have been dis¬ 
cussed under the heading of Tumors of the Brain. 

4. Syphilitic Endarteritis. —The syphilitic changes in the 
walls of the cerebral arteries were described by Huebner in 
1874, and the lesion is known as “ Huebner’s arteries.” 


SYPHILIS OF THE BP A IN. 


7S7 


The lesion consists in a thickening of the intiina by con¬ 
nective tissue, in some cases leading even to an obliteration 
of the lumen. Areas of softening may occur in the brain- 
tissue, from the obliteration of the lumen of the vessel by 
this new growth or by thrombus-formation. The middle 
cerebral artery is the one most usually and most exten¬ 
sively affected. The symptoms resemble those of cere¬ 
bral endarteritis. Syphilitic stupor and paralysis require 
special description. 

Syphilitic Stupor .—The patient complains of severe noc¬ 
turnal headache, and after a time passes into a peculiar 
somnolent condition ; he may lie for days apparently asleep, 
or may sit for hours at a time in a torpid, dazed state of 
mind, answering questions in a peculiar, slow, automatic 
way, as though talking in his sleep. From time to time 
the patient may wander about in an aimless fashion. The 
evidences of severe headache are usually marked, even 
during the periods of stupor. Prolonged stupor is of seri¬ 
ous import, but is not incompatible with complete recovery. 
The majority of cases, unless relieved by treatment, sud- 
dently pass into a condition of profound coma, which is 
usually fatal. 

Syphilitic paralysis comes on suddenly, without loss of 
consciousness and without exciting cause. The paralysis, 
which is not complete, and is of a transitory, fugitive charac¬ 
ter, may be of irregular distribution or may be hemiplegic 
in type. Oculo-motor paralysis is not uncommon. These 
fugitive palsies are due to functional brain-disturbance from 
the diminished blood-supply through the narrower arteries. 
Should thrombus occur, softening will ensue, so that the 
paralysis becomes permanent. 

5. Syphilitic disease of the brain may present nearly the 
clinical picture of general paresis. The exact pathology 
of these cases, however, is not known, and it cannot be 


788 MANUAL OF THE PRACTICE OF MEDICINE . 

asserted as yet that this form of syphilitic brain disease is 
an independent affection. 

The prognosis is, upon the whole, favorable, although it 
should be guarded. More or less recovery is to be expected 
unless the symptoms indicate an absolute destruction of 
brain-tissue. 

Treatment consist in the vigorous employment of anti¬ 
syphilitic drugs. Mercury should at once be ordered by 
inunction, and pushed until the “ gums are touched.” Sali¬ 
vation, however, should always be avoided. 

Potassium iodide in 30-grain doses three times a day, 
largely diluted in water or milk, should be pushed rapidly 
until 300 grains daily are taken, unless the patient show 
such dangerous symptoms of iodism as hemorrhages. In 
cases of sudden coma timely venesection may be the means 
of saving life. 


4. DISEASES OF THE SPINAL CORD. 

( a ) Affections of the Meninges. 

DISEASES OF THE DURA MATER. 

Pachymeningitis externa occurs in an acute and in a 
chronic form. The acute cases regularly are secondary to 
inflammation of the vertebral bones or to the extension of 
neighboring abscesses. The inflammation is fibrino-purulent 
and gives the symptoms of a compression-myelitis. 

Chronic external pachymeningitis is usually due to 
tubercular disease of the vertebrae. The external layer of 
the dura is rough, thickened, and covered with cheesy 
material. 

The symptoms are due to irritation and compression of 
the anterior and posterior nerve-roots (hyperaesthesia and 



DISEASES OF THE DURA MATER. 


789 


motor spasms, anaesthesia, paralysis, atrophy of muscles, and 
loss of reflexes) and to slow compression of the spinal cord 
(loss of motion and sensation below the lesion). 

Treatment is that of the original disease and that of 
myelitis. 

Pachymeningitis Interna PLemorrhagica (Haematoma 
of the Dura Mater).—This disease is usually associated with 
a similar affection of the dura mater of the brain, and the 
two lesions are identical, so that a further description of the 
disease process is not necessary. The cervical region is the 
one usually affected. The symptoms are those of chronic 
spinal meningitis—pain in the back, motor and sensory irri¬ 
tation and impairment. Hemorrhages occur from time to 
time, causing sudden exacerbations of the spinal symptoms 
and compression-symptoms (see Meningeal Hemorrhage). 

Treatment is unavailing. 

Pachymeningitis Interna Hypertrophica. —The dura 
becomes thickened by fibrous tissue, which irritates and de¬ 
stroys the nerve-roots and causes slow compression of the 
cord. The thickening of the dura generally extends above 
the cord like a ring, and is usually limited to the cervical 
region. 

Symptoms.— 1. Stage of Irritation .—The symptoms are 
due to irritation of the anterior and posterior nerve-roots. 
Neuralgic pains develop in the course of the affected nerves, 
and are referred to the neck, arms, and the upper portion of 
the thorax. There are areas of hyperaesthesia with tingling 
sensations. Motor symptoms consist of spasm and rigidity 
of the neck and of the muscles of the upper extremities. 

2. Stage of Destruction .—Hyperaesthesia and neuralgia 
give way to anaesthesia. Paralysis with atrophy and loss 
of reflex succeeds the muscular spasms. Deformities result 
from the atrophy and paralysis. If the lower cervical en¬ 
largement be compressed, the ulnar and median nerves are 


790 MANUAL OF THE PRACTICE OF MEDICINE . 

chiefly affected, so that over-extension of the hand results. 
If the lesion be higher up, the musculo-spiral nerve is 
affected, so that the hand will drop. Secondary degenera¬ 
tion of the pyramidal tract results from the pressure-myelitis, 
and spastic paraplegia develops (see Secondary Lateral 
Sclerosis). 

The prognosis is bad for recovery, although death usually 
results from intercurrent disease. In some cases the dis¬ 
ease may be arrested, and the patient live for years with 
permanent contractures and deformities. 

Treatment consists of counter-irritation to the affected 
portion of the spine, and the empirical use of potassium 
iodide. 

DISEASES OF THE PIA MATER. 

Acute Leptomeningitis. 

Etiology.—Acute inflammation of the pia covering the 
cord may be due to extension of a similar inflammation of 
the pia of the brain, being thus part of the lesion of a simple 
or an epidemic meningitis ; or it may be due to traumatism 
of the vertebrae, or to operation, such as the opening of a 
spina bifida. The disease may complicate certain acute 
infectious diseases, especially pneumonia, small-pox, scarlet 
fever, and typhoid fever. A tubercular inflammation of the 
spinal meninges may also occur. In a few cases the excit¬ 
ing cause seems to be exposure to wet and cold. The in¬ 
fecting germ may be that of epidemic cerebro-spinal men¬ 
ingitis (g. v.), the cocci of pus, the pneumococcus, or 
Eberth’s bacillus. 

Pathology.—The lesions may be diffused throughout the 
length of the cord or may be localized in the cervical region. 
The pia is congested, thickened, and infiltrated with fibrin, 
serum, and pus. The exudation is usually more abundant 
in the posterior portions of the pia, owing to gravitation 


DISEASES OE THE PI A MATED . 791 

when the patient lies upon his back. The peripheral por¬ 
tions of the cord are usually infiltrated by inflammatory 
products. The nerve-roots may also be involved. In the 
majority of cases similar lesions are found in the cerebral 
pia mater. 

The symptoms are due in the first stage to intense irrita¬ 
tion of the spinal nerves. Pain in the back and shooting 
pains along the nerves, with areas of hyperaesthesia, are the 
prominent sensory symptoms. Irritation of the motor nerves 
gives rise to spasm and rigidity of the affected muscles. 
The spine is stiff and rigid; the head is thrown back; there 
may be opisthotonos. Owing to the retraction of the head 
and neck, the larynx may be so firmly pressed against the 
spinal column as to cause obstructive dyspnoea with stridor. 
The reflexes are generally exaggerated. There may be reten¬ 
tion of urine from reflex spasm of the bladder. During the 
earlier stages there is no paralysis, though the muscles may be 
kept quiet, so as not to increase the neuralgic pains. Fever is 
regularly present, but runs an atypical course, rarely ex¬ 
ceeding 104° F. Finally the second stage develops, in 
which hyperaesthesia is succeeded by anaesthesia, the pains 
cease, and complete paralysis supervenes. There may now 
be developed bed-sores and paralysis of the sphincters. 
Reflex irritability becomes lost. 

The diagnosis may be difficult. Symptoms of spinal 
meningitis may be present in cases in which the meninges 
are afterward demonstrated to be normal, while well-marked 
cases of leptomeningitis, especially of the cerebro-spinal 
form, may be unattended by characteristic symptoms. The 
diagnosis from tetanus is made by the absence of trismus 
and of the risus sardonicus and by the intensity of the pains. 
Myelitis is to be excluded by the marked and continued 
hyperaesthesia, by the late appearance of paralysis, and by 
the bladder not being involved. 



792 MANUAL OF THE PRACTICE OF MEDICINE . 

The prognosis is not good, although the acute condition 
may subside and symptoms of chronic meningitis develop. 
Dyspnoea the result of spasm or paralysis of the re¬ 
spiratory muscles is a most unfavorable symptom. 

The treatment is practically that of acute myelitis. 

Chronic Leptomeningitis. 

Etiology.—Chronic spinal meningitis may follow an acute 
attack or may be chronic from the start. In the latter case 
the disease may be due to syphilis or alcoholism, or the 
lesion may complicate chronic diseases of the cord that ex¬ 
tend so as to involve the membranes, or extra-medullary 
lesions, such as tumors or disease of the vertebral bones. 

Pathology.—When the condition follows an acute attack, 
the lesions usually involve an extensive area of the mem¬ 
branes ; in other cases, chronic from the start, the distribu¬ 
tion is more limited. The pia is thickened and adherent to 
the cord and the dura. The nerve-roots may be compressed, 
and may even become atrophied. The cord usually shows 
increase of connective tissue in the cortical zones. 

The symptoms resemble in kind those of the acute form, 
and are due to the involvement of the nerve-roots, but mus¬ 
cular spasms are much less prominent. There is pain in 
the back, radiating along the course of the nerves, with 
areas of hyperaesthesia. Stiffness of the back and generally 
increased reflexes are present in the earlier stages. The 
rectum and the bladder are but seldom involved. Motor 
weakness gradually merges into paralysis, with atrophy of 
the muscles and loss of reflexes. These symptoms result 
from atrophy of the anterior nerve-roots through compres¬ 
sion by the thickened pia. The symptoms of meningitis are 
frequently accompanied by those due to a primary disease 
in or outside of the spinal cord. 


HEMORRHAGE INTO THE SP/NAl MEMBRANES . 793 


Prognosis.— The disease is chronic in its course, extend¬ 
ing over years. Recovery cannot be expected. 

Treatment is that of the chronic stage of myelitis. 

Hemorrhage into the Spinal Membranes. 

Etiology and Synonyms.— This rare condition may re¬ 
sult from (1) blows and concussions, (2) chronic pachymenin¬ 
gitis haemorrhagica, (3) rupture of an aortic aneurysm into 
the spinal column after erosion of the vertebral bones, (4) 
hemorrhagic diseases, as purpura haemorrhagica, and scurvy, 
(5) after convulsions or tetanus, (6) or as a lesion of caisson- 
disease. Blood effused into the cranium, as in hemorrhages 
at the base, may make its way down between the membranes 
of the cord. This latter diffusion of blood occurs most 
commonly with rupture of an aneurysm of the vertebral or 
basilar artery. Synonyms : Extra-medullary hemorrhage ; 
Haematorrhachis ; Spinal apoplexy. 

Pathology. —The blood may be found between the dura 
and the bones (extra-meningeal hemorrhage), and is extrav- 
asated from the large plexus of veins lying outside the dura. 
In other cases the blood is found between the membranes 
(intra-meningeal hemorrhage). Hemorrhage is most com¬ 
mon in the cervical region, but it may occur anywhere. In 
extensive extravasations the spinal cord may be com¬ 
pressed, but the amount of blood is rarely sufficient for this. 

Symptoms. —The characteristic features of hemorrhage 
within the spinal membranes are the sudden appearance of 
symptoms of an intense meningeal irritation without initial 
fever. Pain develops suddenly in the back and radiates 
along the course of the nerves. There are muscular rigidity 
and spasm. Motor and sensory impairment may ultimately 
appear, but seldom to a great extent. If the hemorrhage 
be in the cervical region, the pain is felt in the arms, the 
neck is rigid and immobile, and dysphagia, interference 






794 MANUAL OF THE PRACTICE OF MEDICINE. 

with respiration, and dilatation of the pupils may appear. 
Larger hemorrhages in the upper cervical region may be 
immediately fatal. Occurring in the dorsal region, the pain 
encircles the abdomen. Hemorrhage in the lumbar region 
causes pain in the legs; there may be spasmodic retention 
of urine. If the hemorrhage compress the cord, compres¬ 
sion-myelitis will result, with paraplegia and anaesthesia, and 
the rectum and bladder will be involved. 

The prognosis is bad, but not hopeless. Perfect recovery 
may follow slight extravasations. 

Treatment.—The patient should lie on the face while 
ice-bags are applied to the spine. Ergot may be given at 
the onset in full doses. After the hemorrhage has ceased 
the treatment is that of myelitis. 

(b) Diseases of the Blood-vessels. 

ANAEMIA. 

The etiology and symptomatology of spinal anaemia are 
but little known. In profound anaemia there may be no 
symptoms referable to the cord. It is known that ligature 
of the abdominal aorta in animals is followed by paraplegia, 
and in man this paralytic condition has followed sudden 
blockage of an aneurysm of the abdominal aorta by a 
thrombus or by a detached portion of the clot. A transient 
paraplegia has also followed sudden and profuse hemorrhage 
or exhausting diarrhoea. The weakness of the legs in those 
suffering from aortic regurgitation is supposed to be due to 
spinal anaemia. 

HYPEREMIA. 

Acute hypercemia results from sexual excesses, physical 
over-exertion, sudden cessation of the menses, and from 
over-dosing by strychnine. 

The symptoms are indefinite. There may be numbness, 


HEMORRHAGE INTO THE CORD. 


795 


with neuralgic pains, muscular twitching, and weakness, 
these being usually confined to the lower extremities. 

Treatment consists in the application of an ice-bag or of 
cups to the spine. The patient should lie on the side or the 
face. Sodium bromide may be given to control the symp¬ 
toms. Ergot, although recommended by some, does not 
seem to be of as much service as is generally supposed. 

Chronic hypercemia may complicate various lesions of the 
cord and membranes, but the symptomatology is obscure. 

HEMORRHAGE INTO THE CORD. 

Etiology and Synonyms.—Hemorrhage into the cord 
has been found with tetanus, strychnine-poisoning, and 
conditions leading to sudden asphyxia. Hemorrhage 
commonly complicates inflammations and tumors of the 
cord. Primary hemorrhage, which may be due to blows 
or falls, to convulsions, or to hemorrhagic conditions, is 
most common in young males. Synonyms: Haemato- 
myelia; Intramedullary hemorrhage; Spinal apoplexy. 

Pathology.—The clot is rarely larger than an almond, 
and is usually situated in the central gray matter. The 
nerve-structures are lacerated at the seat of hemorrhage, re¬ 
sulting in a total transverse destructive lesion of the cord. 

The symptoms resemble those of acute transverse mye¬ 
litis, but there is no initial fever, the paraplegia is suddenly 
induced, and the stage of irritation is not marked. The 
case may resemble one of spinal meningeal hemorrhage, but 
in the latter condition pains and spasm are more marked 
than anaesthesia and paraplegia, and there is more liability 
of recovery. 

The ultimate course of spinal hemorrhage is that of a 
chronic transverse myelitis, and in many cases it is impos¬ 
sible to say whether the case is one of primary hemorrhage 
with myelitis or of myelitis with secondary hemorrhage. 


796 MANUAL OF THE PRACTICE OF MEDICINE. 

The prognosis is not good. Many cases die during the 
acute symptoms, while others live for years with permanent 
paraplegia. In these cases the prognosis is that of chronic 
myelitis. 

The treatment is that of myelitis. 

Embolism and thrombosis are rare conditions. Em¬ 
bolism may be suspected, should a patient with valvular 
disease suddenly develop paraplegia and paranaesthesia with¬ 
out other apparent cause. 

CAISSON-DISEASE; DIVER’S PARALYSIS. 

Etiology.—Persons who work in caissons and diving- 
bells under an increased atmospheric pressure may develop 
this disease when they suddenly emerge into the normal 
atmosphere. The pressure must be more than three atmo¬ 
spheres, and the longer they work in the caisson and the 
more suddenly they return to the surface, the greater is the 
liability to the disease. Those unused to the work are most 
frequently attacked. 

The pathology is somewhat obscure. Under raised 
atmospheric pressure the blood is driven from the surface 
to the internal organs. When the pressure is reduced to 
the normal, vascular disturbances are supposed to result in 
the cord, with spots of congestion and small hemorrhages 
which may ultimately result in myelitis. Another theory 
is that an excess of nitrogen is absorbed by the blood when 
under high pressure, and that when the pressure is too sud¬ 
denly reduced bubbles of this gas are liberated and lacerate 
the nerve-structures of the cord. 

The symptoms may appear at once or may be deferred 
half an hour or more after leaving the. caisson. In most 
cases there are agonizing neuralgic pains in the limbs, the 
legs are tender to the touch, and there is some loss of 


ACUTE ANTERIOR POLIOMYELITIS . 


797 


motor power. There are apt to be epigastric pain, nausea, 
vomiting, headache, and dizziness. In severe cases paralysis 
and anaesthesia rapidly develop in the legs, although neur- 
algic pains may still continue, d here may be temporary 
loss of consciousness. 

Prognosis. — The patient may convalesce in a few days, 
or recovery may result only after weeks or months of suf¬ 
fering and paralysis. Severe cases may pass into coma, 
and die in a few hours or days after the onset. Atrophic 
bed-sores and cystitis may complicate the course of the 
protracted cases. In some instances the patient is left 
with permanent paraplegia and the symptoms of transverse 
myelitis. 

Treatment. —A sufficient time must be spent in passing 
through the lock, in which the pressure is reduced. At 
least five minutes should be spent for each atmosphere. 
Workmen should be carefully selected and gradually accus¬ 
tomed to the work, and the hours of labor in the caisson 
should at first be short. When the symptoms occur, it is 
recommended that the patient should at once be put back 
under a slight atmospheric pressure. The use of ergot in 
large doses seems to be of service during the acute stages 
of the disease. Morphine may be required for the neural¬ 
gic pains. The paralytic symptoms are to be treated on 
the same principles as those governing the treatment of 
myelitis. 

(y) Diseases of the Substance of the Cord. 

ACUTE ANTERIOR POLIOMYELITIS (ATROPHIC 

SPINAL PARALYSIS). 

Acute anterior poliomyelitis occurs both in children and 
in adults. An infantile and an adult form are to be 
described. 


798 MANUAL OF THE PRACTICE OF MEDICINE. 

Anterior Poliomyelitis in Children. 

Etiology and Synonym.—The disease occurs in children 
between two and five years of age, and is equally frequent 
in boys and girls, in weakly and in robust subjects. The 
majority of cases appear during the warm summer months. 
There may be a history of exposure to the hot sun, of a 
fall or an injury, or the condition may follow some acute 
infectious disease, especially measles. In some instances it 
would seem that the disease itself was of an infectious 



Fig. =9. —Diagrammatic representation of the symptoms that result from acute destruc¬ 
tion of the anterior cornua of the spinal cord (Bramwell). On the left side the destruction 
of the nerve-cells is complete : the anterior nerve-roots, motor nerve-fibres, and the muscles 
which they supply are all degenerated; there is a total “ block ’ to the passage of voluntary 
motor and reflex motor impulses. On the right side two-thirds of the motor cells are de¬ 
stroyed ; two-thirds of the muscular area connected with the right anterior cornu are degen¬ 
erated and atrophied; one-third (M) remains healthy, and can be made to contract by 
voluntary or reflex motor impulses. 

origin, and epidemics of the disease have even been re¬ 
corded. Synonym: Infantile paralysis. 

Pathology. —The lesion consists in the degeneration of 
the anterior motor cells, preferably of the lumbar and cer- 







ACUTE ANTERIOR POLIOMYELITIS. 


799 


vical enlargements. The ganglionic cells become swollen 
and degenerated, and may either return again to a normal 
condition or may become atrophied. 

During the earlier stages the gray matter about the motor 
cells becomes congested and infiltrated by leucocytes; later 
the inflammation becomes chronic and results in an in¬ 
creased production of connective tissue. As the anterior 
motor cells preside over the nutrition of the anterior nerves 
and the muscles to which they are distributed, granular 
degeneration and atrophy of nerve and of muscle follow 
the destructive lesion of the motor cells. The lesion is 
usually bilateral, and affects groups of cells functionally 
associated (Remak describes an “ upper-arm type,” in which 
the supinator longus is paralyzed, with the biceps and the 
brachialis anticus). Through the anterior motor cells pass 
fibres from the central regions of the cord, controlling vas¬ 
cularity and general nutrition, so that destructive lesions of 
the anterior cells are regularly followed by imperfect 
growth, cyanosis, and a lowered temperature of the affected 
members. 

In cases of long standing the affected cornua become 
small and atrophied, and slight sclerotic changes are found 
in the pyramidal tract. 

The symptoms may be divided into three stages: 

1. The Stage of Onset .—The onset begins abruptly, with 
fever of from ioo° to 103° F., usually accompanied by con¬ 
vulsions, twitching of the muscles, delirium, or even coma. 
There may be, in older children, some complaint of aching 
in the joints. The symptoms may be well marked, or there 
may be only moderate fever which may pass unnoticed. 
The symptoms of this stage last for a few hours or for 
several days. 

2. The stage of paralysis is distinctive in that the greatest 
degree of paralysis is reached at the onset, and any change 


800 MANUAL OF THE PRACTICE OF MEDICINE. 


afterward is for the better. When the paralysis has remained 
stationary for twenty-four hours the danger of further ex¬ 
tension is extremely small. The distribution of the paral¬ 
ysis depends upon the situation and extent of the lesion. 
The type is paraplegic, and the legs are more frequently 
affected than the arms, in the proportion of 4: 1. One or 
both legs may be paralyzed, or the muscles of the upper 
extremities may be affected as well, or may be paralyzed 
alone, or one arm and one leg may be involved. The 
paralyzed muscles are those functionally associated. The 
extensors are more frequently involved than the flexors. 
All the muscles of a limb are but rarely affected. After a 
stationary period of from two to six weeks some of the 
paralyzed muscles acquire their former power, while others 
remain paralyzed. The affected muscles are flabby, undergo 
wasting, and there is absence of all reflex action. Fibrillary 
twitchings may occur in the paralyzed parts, and the skin 
is bluish and cold to the touch. The affected muscles 
show the reaction of degeneration, 1 there being at first an 

1 Reaction of Degeneration (R. D.).—Since contractions only occur on clos¬ 
ing or opening the galvanic current, and as there are but two poles, the anode 
or positive and the cathode or negative, there are of necessity but four possible 
forms of contraction : 

1 . When the cathode is on the muscle and the anode upon a neutral and 
distant point— (a) the contraction which occurs on closing the current (the 
cathodal closure contraction, or C. C. C.); (6) the contraction which occurs 
on opening the current (cathodal opening contraction, or C. O. C.). 

2 . When the anode is on the muscle and the cathode upon a distant neutral 
point—(fl) the contraction which occurs on closing the current (anodal closure 
contraction, or A. C. C.); (h) the contraction which occurs on opening the 
current (anodal opening contraction, or A. O. C.). 

These four forms of contraction occur in a definite order of intensity, which 
order differs in health and in disease. In health the order is—C. C. C.- 
A. C. C.-A. O. C.-C. O. C. 

The A. O. C. and the C. O. C. are usually evident only with currents of 
such intensity as to cause pain. 

In degeneration of the anterior nerve or of the motor cells of the anterior 



ACUTE ANTERIOR POLIOMYELITIS. 


801 


increase and then a decrease in the galvanic irritability, and 
in two weeks or sooner there is a total loss of faradic ex¬ 
citability. 

Negative symptoms are important: (i) There is no 
secondary involvement; (2) the bladder and the rectum are 
unimpaired; (3) trophic changes in the skin do not occur; 
(4) there is no change in the mental condition nor in the 
general health; (5) the cranial nerves are not involved. 

3. Symptoms of permanent deformity are due (1) to the 
condition of the paralyzed limb—the growth is retarded, 
the limb appears atrophied, withered, cold, and bluish; (2) 
to increased mobility of the joints, owing to the relaxed con¬ 
dition of the paralyzed muscles; (3) to muscular contracture 
of the unparalyzed muscles, the type of which deformity is 
club-foot. 

The prognosis for life is good, but perfect recovery from 
paralysis is not to be expected, although a certain amount 
of improvement almost always occurs. The following rules 
may be given in the way of estimating the extent of perma¬ 
nent paralysis: Muscles which in two weeks respond to 
faradism will surely recover, while muscles not thus respond¬ 
ing will remain paralyzed for a greater or less time. Mus¬ 
cles which in three months show a return of irritability to 
faradism will recover partially. Muscles which do not re¬ 
spond to faradism in six months will never recover. 

It is important never to give too gloomy a prognosis as 
long as the faintest contraction is produced by the faradic 
current. 

Treatment. —During the stage of onset the spine should 
be cupped and fever be controlled by the ordinary measures. 
A brisk laxative should be given at the onset. During the 

cornua the order is changed to the “reaction of degeneration,” in the follow¬ 
ing order of intensity: A. C. C.—C. C. C.-C. O. C.—A. O. C. The character 
of the contraction is also changed, being slow, prolonged, and even tetanic. 

51 


802 manual of the practice of medicine. 


earlier part of the stage of paralysis ergot and sodium bro¬ 
mide with small doses of potassium iodide should be given 
until some amount of improvement appears. During this 
time the paralyzed members should be wrapped in cotton. 
In two or three weeks, when the acute stage has passed, 
strychnine should be administered, as in the following 
prescription: 


R Strychnine sulphat., gr. ; 

Ferri pyrophosphat., gr. j ; 

Acid, phosphoric, dil., Til iv ; 

Syrup, zingiberis, ad 3j.—M. 

Sig. Such a dose three times a day to a child from three 
to five years of age. 


The affected parts should be carefully and persistently 
rubbed morning and evening, and the muscles should at 
the same time be gently kneaded. The faradic current 
should be applied daily to such muscles as respond, while 
to the paralyzed muscles the slowly interrupted galvanic 
current should be applied. 

For the permanent deformities much good can be done 
by various apparatus or by surgical measures. 


Anterior Poliomyelitis in Adults. 

Males are more usually affected than females. The etiol¬ 
ogy and pathology are the same as in children, but the fol¬ 
lowing clinical differences are observed: (i) The onset is 
less acute; (2) the cranial nerves may be involved in some 
cases ; (3) rheumatoid pains may be present, and are referred 
to the affected muscles and joints; (4) muscular tenderness 
may be extreme; (5) fewer muscles are affected than in 
children, and recovery is usually more complete ; (6) owing 
to the development of the limbs of an adult, the withering 


SUBACUTE AND CHRONIC POLIOMYELITIS. 803 

and retarded growth of the affected member are not so 
noticeable. 

Although the adult cases of anterior poliomyelitis are 
described as the counterpart of the same disease in children, 
there is strong probability that the disease is really a multi¬ 
ple neuritis. Further observations are necessary to deter¬ 
mine this point. 

SUBACUTE AND CHRONIC POLIOMYELITIS. 

Synonym.— Duchenne’s paralysis. 

It is undecided whether this disease is a chronic polio¬ 
myelitis or a multiple neuritis. The pathology is therefore 
obscure. 

Etiology.—The disease is rare, and is almost exclusively 
confined to adults. 

Symptoms. —The onset is gradual, and is characterized 
by motor weakness which increases in extent and ultimately 
leads to paralysis. The paralyzed muscles rapidly atrophy, 
show absence of reflexes, and the R. D. can be obtained. 
There is no sensory involvement, nor is the bladder or the 
rectum implicated. The symptoms usually begin in the 
legs and extend to the trunk and the upper extremities 
(ascending type); or the disease may be first noticed in the 
arms, and may spread to the legs (descending type). The 
early stages of the descending type, in which the arms are 
first affected, may closely resemble lead-paralysis. 

Prognosis. —In the majority of cases a certain degree of 
improvement is noticed in a few weeks or months, but 
recovery is incomplete except in rare cases. In some 
instances death results from an extension of the disease to 
the medulla, with the symptoms of bulbar paralysis. The 
duration of the disease is usually from one to four years. 

Treatment is that of the acute poliomyelitis after the 
febrile stage has passed. 


804 manual of the practice of medicine. 

PROGRESSIVE MUSCULAR ATROPHY. 

Etiology and Synonyms. —The disease is most frequent 
in males between twenty-five and forty-five years of age. 
An hereditary influence is often observed, and there are cases 
in which the disease has been handed dov/n for five genera¬ 
tions. It is possible that some of these hereditary cases, 
however, are really examples of idiopathic muscular 
atrophy. Excessive physical exertion, mental worry, expos¬ 
ure to wet and cold, syphilis, and chronic lead-poisoning 
have been ascribed as exciting causes ; the affection has been 
known to follow measles, typhoid fever, and acute rheuma¬ 
tism. Synonyms: Wasting palsy; Chronic anterior polio¬ 
myelitis. 

Pathology.— The lesions are found in the muscles, nerves, 
and cord. The muscles are wasted and pale, and the fibres 
are shrunken. Certain fibres are seen to have entirely disap¬ 
peared, leaving empty and collapsed sheaths. The wasting 
of the muscle is not en masse , but fibre after fibre is picked 
out in the process of atrophy. There may be an increase 
in the interstitial tissue. The atrophy of the fibres is simple, 
and granular degeneration is not apparent as in infantile 
paralysis. The anterior nerve-roots emerging from the 
affected part of the cord undergo simple atrophy, and fibre 
after fibre disappears. In the cord the lesion is practically 
confined to the anterior cornua. The motor ganglionic cells 
waste, lose their processes, and one after another undergoes 
simple atrophy (Fig. 60). Sclerotic changes are usually 
found in the direct and crossed pyramidal tract, and when 
these changes are sufficiently marked to give rise to symp¬ 
toms, the name of “ amyotrophic lateral sclerosis ” is given 
to the resulting complex lesion. This form of disease will 
be separately considered. In many cases the disease extends 
upward to involve the motor nuclear cells in the medulla. 


PROGRESSIVE MUSCULAR ATROPHY 


805 


The symptoms begin gradually and insidiously. It is 
noticed that the muscles tire easily, are not as firm as nor¬ 
mal, and ache after slight exertions. Fibrillary contractions 



Fig. 60. —Diagrammatic representation of the symptoms that result from slow destruction 
of the multipolar nerve-cells of the anterior cornu (Bramweli). On the left side the disease 
is in an early stage. One nerve-cell (a 1 ) is completely destroyed. Its muscular fibre (1') is 
completely atrophied Voluntary motor and reflex motor impulses are “blocked” at the 
seat of the lesion (a'). One nerve-cell ( b’) and its muscular fibre (2') are very much atro¬ 
phied, hut feeble motor and reflex impulses can still pass through the cell to the muscle. 
Two nerve-cells {c'c') are healthy. Their muscular fibres are of normal bulk, and can be 
made to contract either by voluntary or reflex impulses. On the right side the disease is 
much more advanced. The muscular area is three-fourths degenerated There is a total 
“block” at a and a. This condition represents a late stage of progressive muscular atro¬ 
phy. The atrophy of the muscular fibres is represented as simple. 


may be observed. The atrophy is usually first noticed in 
the interossei muscles and in those of the ball of the thumb. 
Motor weakness is proportionate to the extent of the 
atrophy, as there is in this disease no essential paralysis. 
Advanced atrophy of the interossei give the hand the 
“ griffin-claw ” appearance, in which flexion of the last two 
phalanges is associated with extension of the first phalanx 
at the metacarpal joint. Occasionally the deltoid is the first 









8o6 MANUAL OF THE PRACTICE OF MEDICINE. 


muscle to suffer, and its atrophy may present a deformity 
of contour closely resembling a subglenoid dislocation of 
the humerus. 

In go per cent, of the cases the disease begins in the hand 
or shoulder. More exceptionally the affection may first 
show itself in the lumbar or abdominal muscles, and still 
more rarely in the muscles of the legs. The atrophied 
muscles are flaccid, and usually retain their normal elec¬ 
tric reactions, for what muscle is left is good. In late 
cases, however, with rapid atrophy the R. D. may finally 
appear. Reflexes are diminished according to the amount 
of the atrophy. Fibrillary twitchings are not infrequently 
present. Atrophy proceeds from muscle to muscle in 
the order of the juxtaposition of their nerve-nuclei in 
the cord. Bilateral symmetry is usually preserved, al¬ 
though the wasting may be more marked on one side 
than the other. Owing to the contracture of unparalyzed 
muscles various deformities result; the “griffin-claw,” or 
“ main de griffe,” has already been described. When the 
lumbar muscles are implicated the back is arched and the 
line of gravity falls behind the sacrum. When the abdom¬ 
inal muscles are affected the back is also arched, but the 
line of gravity falls in front of the sacrum. 

In course of time all the voluntary muscles may become 
implicated, so that the patient is practically reduced to 
“ skin and bone.” The normal appearance of the facial 
muscles is in strong contrast to the wasting of the rest of 
the body. Ophthalmoplegia externa and bulbar paralysis 
may develop toward the close of the disease. 

The diagnosis of “ main de griffe ” from lesion of the ulnar 
nerve is made by the absence of sensory symptoms. The 
diagnosis from idiopathic muscular atrophy is to be made 
by the different order of distribution of the atrophies in the 
latter disease, and by the fact that the latter condition usually 


AMYOTROPHIC LATERAL SCLEROSIS. 807 

occurs in young children. Amyotrophic lateral sclerosis is 
to be excluded by the absence of spasm and rigidity. 

Prognosis.— The course of the disease is usually progres ¬ 
sive. Death may result from exhaustion, from bulbar paral¬ 
ysis, or from respiratory affections. The disease may be¬ 
come quiescent at any time, and the patient may live for 
years. These cases are often seen as freaks in museums, 
under the name of “ living skeletons.” 

Treatment is of no avail. The general nutrition of the 
muscles should be maintained by massage and electricity, 
and strychnine, arsenic, and nitrate of silver may be given 
internally. If the muscles of respiration be affected, extra¬ 
ordinary care should be taken to avoid cold, as even a 
trifling bronchitis may terminate fatally. 

AMYOTROPHIC LATERAL SCLEROSIS. 

Etiology.—This condition is really one of progressive 
muscular atrophy in which sclerosis in the lateral columns 
is sufficiently marked to produce symptoms, and is not at 
present regarded as an independent disease. The etiology 
is therefore the same as that of progressive muscular atrophy, 
except that the disease may occur after the age of seventy 
as a senile change. 

Pathology.—The lesions are the same as those of pro¬ 
gressive muscular atrophy, except that the direct and crossed 
pyramidal tracts show degeneration and sclerotic change, 
and the motor nuclear cells of the pons and of the medulla 
are more frequently involved. 

The symptoms result from the combination of progres¬ 
sive muscular atrophy and lateral sclerosis. Wasting and 
weakness progress, with rigidity, contractures, and exagger¬ 
ated reflexes. In the hands and arms the atrophy and weak¬ 
ness are especially well marked, while in the legs typical 
spastic paraplegia develops early. Fibrillary twitchings of 


8o8 MANUAL OF THE PRACTICE OF MEDICINE . 

the muscles are commonly observed. There are no sensory 
disturbances, and the bladder and the rectum are under full 
control. Ultimately the rigidity and muscular wasting be¬ 
come general, paralysis results, and symptoms of bulbar 
paralysis or of ophthalmoplegia externa make their appear¬ 
ance. 

The prognosis is not as good as in progressive muscular 
atrophy, as the disease is seldom if ever arrested. Death 
results in from one to four years. 

Treatment is of no avail. Long-continued rest in bed 
has been recommended. 

BULBAR PARALYSIS. 

Synonym.—Glosso-labio-laryngeal paralysis. 

Two forms of bulbar paralysis are recognized—the acute 
and the chronic. 

1. Acute bulbar paralysis results (i) from small hemor¬ 
rhages into the medulla; (2) from areas of softening follow¬ 
ing embolism or thrombosis; (3).from an acute inflamma¬ 
tory affection analogous to anterior poliomyelitis; (4) as a 
terminal lesion of Landry’s paralysis. The lesion is almost 
regularly bilateral. 

The symptoms are those of the chronic form, differing 
only in their acuteness of onset. There may be hemiplegia 
or crossed facial paralysis. These acute cases prove rapidly 
fatal, although in rare instances the condition may become 
chronic. 

2. Chronic bulbar paralysis is commonly associated with 
similar degeneration of the motor cells of the spinal cord. 

The condition is rare before the age of forty, and usually 
appears as the terminal event of progressive muscular 
atrophy, of amyotrophic lateral sclerosis, or of Duchenne’s 
paralysis. 

Symptoms.—There is a progressive palsy of the tongue, 


BULBAR PARALYSIS. 


809 

lips, palate, pharynx, and laryngeal muscles, resembling in 
character the muscular changes of progressive muscular 
atrophy. The tongue becomes tremulous and is protruded 
with difficulty, and finally the lingual and dental consonants 
d y /, n, r, and t cannot be pronounced. The tongue atro¬ 
phies. Chewing and swallowing are impaired. The lips be¬ 
come paralyzed and tremulous, the patient cannot whistle, 
and the lip-letters b,f v, o t and 11 cannot be pronounced. 
Saliva drools from the mouth. There may be an emotion¬ 
less expression, from facial paresis and atrophy. The 
pharynx becoming paralyzed, food regurgitates or cannot 
be swallowed. The laryngeal muscles waste, so that the 
voice is weak, almost inaudible, but extreme degrees of 
abductor paralysis are rare. Cough becomes impossible, 
and, the larynx being unprotected, aspiration- or deglutition- 
pneumonia is rendered possible. There are no sensory 
symptoms, and the mind is clear though emotional. Taste 
is not impaired. Pulmonary and cardiac crises occur when 
the nucleus of the vagus is affected. Severe dyspnoea 
appears on exertion, and, later, furious spontaneous attacks 
of suffocation, with cyanosis and a sense of extreme fulness 
in the chest, may appear. 

The cardiac crises consist of a rapid and excessively 
feeble heart-action, pallor, anxiety, and a sense of impend¬ 
ing death. 

The diagnosis is not usually one of difficulty. The 
condition, however, may be simulated by a bilateral lesion 
in the lower portion of the third frontal convolution 
(“ pseudo-bulbar paralysis of cerebral origin ”). 

Prognosis.—The duration of the disease is from one to 
four years, with periods of temporary inactivity. Death 
results from inanition, from aspiration-pneumonia, or from 
heart-failure during a cardiac crisis. 

Treatment.—The only thing that can be done is to 


8 10 MANUAL OF THE PRACTICE OF MEDICINE. 


advise the feeding of the patient by the stomach-tube when 
deglutition becomes impaired. 

OPHTHALMOPLEGIA. 

This rare disease is due to the progressive atrophy of the 
nuclei of the cranial nerves of the eye or the eyeball. Ac¬ 
cording to whether the external or the internal muscles are 
affected, there are described ophthalmoplegia externa and 
ophthalmoplegia interna. 

Ophthalmoplegia externa may be found associated with 
general paresis, progressive muscular atrophy, and loco¬ 
motor ataxia, or the nuclear degeneration may be due to 
the pressure of tumors or to basilar meningitis. Mental 
disorders are present in about one-fifth of the cases, and 
atrophy of the optic nerve may coexist. There is a gradual 
loss of power in the extrinsic muscles of the eyeball, start¬ 
ing first in the levator muscles of the lid and in the superior 
recti. The loss of power finally becomes absolute. Ptosis, 
squint, and double vision appear during the earlier stages, 
but later the eyeball becomes fixed and immobile and may 
protrude. The disease is essentially chronic. 

Ophthalmoplegia interna causes loss of pupillary reflex 
and of power of accommodation, and is usually associated 
with locomotor ataxia or with general paresis. The con¬ 
dition may be combined with the external form. Ophthal¬ 
moplegia interna may result from nuclear degeneration or 
from disease of the ciliary ganglion. 

LATERAL SCLEROSIS (SPASTIC PARAPLEGIA). 

Lateral sclerosis may be primary or secondary. 

Primary lateral sclerosis is so rare a condition that by 
some its existence is doubted. It is said to be induced by 
syphilis, over-work, exposure, and sexual excesses, and to 
attack males of middle life. 


L A TER A L SCLER OS/S. 


811 


Secondary lateral sclerosis is the most frequent form of 
spastic paraplegia, and results from any lesion destroying 
the motor cells in the cerebral cortex or cutting off the 
pyramidal fibres from their trophic centres in the motor 
cortical cells. These lesions may be cerebral or spinal. 
Such lesions are—(i) Tumors, softening, or hemorrhage in 
the brain, destroying the motor tract in one hemisphere. 
Secondary sclerosis is found below the lesion in the anterior 
median column and in the opposite lateral pyramidal tract. 
(2) Congenital malformation, hydrocephalus, or bilateral 
meningeal hemorrhage affecting both motor tracts. In 
these cases the descending degeneration is bilateral, involv¬ 
ing both anterior median columns and crossed pyramidal 
tracts. (3) Any lesion in the cord, unilateral or bilateral, 
that separates the fibres of the motor tract from their trophic 
centre in the motor cortex of the brain. Such lesions are 
transverse myelitis, hemorrhage into the cord, or slow com¬ 
pression of the cord by tumor, disease, fracture, or dislocation 
of the vertebra, and meningeal hemorrhage. (4) The lateral 
columns may be involved with other tracts in the cord— 
with the cells of the anterior horns causing amyotrophic 
lateral sclerosis, with the posterior columns causing ataxic 
paraplegia. These combined lesions will be individually 
described. 

Pathology.—The lesion is found to be limited to the 
lateral motor tracts. The anterior median columns may be 
involved in the case of a primary lesion in the brain. There 
is an increase in the connective-tissue framework, and a 
destruction and disappearance of the axis-cylinders of the 
nerve-fibres. 

Symptoms.— Of the Primary Form .—There are first 
noticed a loss of endurance in walking, and stiffness and 
rigidity of the muscles. The muscular weakness is pro¬ 
gressive, and merges into paralysis of voluntary motion. 


812 MANUAL OF THE PRACTICE OF MEDICINE. 


Coincident with the weakness there is a rigidity of the 
affected limbs from a more or less continual spasm of the 
muscles. From time to time clonic spasms occur, especially 
during the night, during which the legs are twitched or 
suddenly jerked out. The gait becomes “ spastic ”—the 
toes stick to the ground, the knees touch or overlap in 
walking, and the leg is in a condition of spasmodic tension, 
or even shows distinct clonus when the ball of the foot rests 
upon the ground. The trunk is usually thrown forward by 
tonic contractures of the calf-muscles, so that crutches or 
canes held far in advance of the body become necessary. 
The power of locomotion is finally lost. The affected 
muscles do not atrophy, and the R. D. is not present. The 
reflexes are regularly increased. The knee-jerk is exces¬ 
sive and prolonged, and may be radiated to the arms or to 
the opposite leg. Ankle-clonus is easily obtained. There 
are no essential sensory symptoms, though there may be 
dull pains in the muscles, and the bladder and rectum are 
not usually involved until late in the disease. Ocular 
symptoms are rare. The arms may escape altogether, or 
rigidity may appear as a late manifestation of the disease. 

Of the Secondary Form .—The symptoms are bilateral or 
unilateral according as to whether one motor tract or both 
are affected. Cerebral lesions usually lead to unilateral 
sclerosis. The symptoms appear rapidly or gradually ac¬ 
cording to the nature of the primary lesion. “ Late rigid¬ 
ity ” with hemiplegia following cerebral hemorrhage is 
synonymous with secondary lateral sclerosis. 

Spastic paraplegia of infants is usually a birth-palsy due 
to meningeal hemorrhage. In other cases the condition 
arises from an arrested development of the pyramidal tracts. 
The symptoms may be bilateral, and the arms are not infre¬ 
quently involved. Idiocy, imbecility, and other mental de¬ 
fects are usually present. 


LOCOMOTOK ATAXIA. 


813 


The diagnosis from hysterical spastic paraplegia may be 
one of great difficulty, as the hysterical form may exactly 
reduplicate the symptoms of the organic disease. In favor 
of the hysterical condition are (1) the sudden development 
of symptoms, (2) the history of hysterical attacks in the past, 
(3) the presence of anaesthesia, hyperaesthesia, or other 
hysterical manifestations, and (4) the sudden remission of 
muscular contractions, which in the organic form should be 
more permanent. 

Prognosis.—The course of the disease is chronic, extend¬ 
ing over many years. The disease is the least fatal of all 
the chronic spinal affections. Its progress may be arrested 
at any time. 

Treatment.—In syphilitic cases mercury and iodide of 
potassium may be tried; strychnine is contraindicated; the 
bromides may be of use in reducing the condition of over¬ 
reflexes ; otherwise there is no medicinal treatment of any 
value. 


LOCOMOTOR ATAXIA. 

Etiology and Synonyms.—This disease occurs in males 
ten times as frequently as in females, and is most common 
between thirty and fifty years of age. Its occurrence under 
the age of twenty-five is rare. The great predisposing cause 
is syphilis, which precedes the disease in two-thirds of the 
cases. Among exciting causes are sexual excesses, great 
physical exertion, and repeated exposures to wet and cold. 
Synonyms: Posterior spinal sclerosis; Tabes dorsalis. 

Pathology.—There is a sclerosis, beginning first in the 
middle zone of the column of Burdach and in the column 
of Lissauer (the narrow marginal zone lying between the 
posterior horn and the pyramidal tract), and extending to 
the column of Goll and the remainder of the column of 
Burdach (Fig. 61). The network of fibres about the vesic- 


8 14 MANUAL OF THE PRACTICE OF MEDICINE. 


ular columns of Clarke are affected by the sclerotic pro¬ 
cesses early in the disease. The lesion begins in the lumbo¬ 
sacral region and extends upward throughout the cord. In 
long-standing cases the sclerosis extends to the lateral 



columns and leads to the degeneration of the pyramidal 
and direct cerebellar tracts. The posterior nerve-roots 
show the lesions of a degenerative neuritis, and become 
small and atrophic. These nerve-changes are frequently 
first observed in the cutaneous filaments, and may even pre¬ 
cede the sclerosis of the posterior columns. The meninges 
over the lateral and posterior columns are thickened and 
abnormally adherent; their blood-vessels show the changes 
of arterio-sclerosis. Besides neuritis there may be muscu¬ 
lar atrophy. Atrophy may occur in any of the cranial 
nerves, especially the optic, third, auditory, and pneumo- 
gastric nerves. There may be sclerosis of the restiform 
bodies or of the inferior peduncles of the cerebellum, or 
sclerotic areas in the hemispheres may resemble the lesions 
of general paresis. 

The disease is not yet thoroughly understood, and three 
theories are advanced to account for the lesions: (i) That 
there is a primary sclerosis of the posterior columns; (2) that 
the sclerosis is dependent upon arterial degeneration of the 
vessels entering the posterior root-zones; and (3) that the 
disease originates in the ganglia of the posterior nerve-roots, 
with secondary degeneration of the sensory fibres entering 









LOCOMOTOR ATAXIA. 


8 i 5 

the cord from these ganglia, with secondary sclerotic changes 
in their course. 

The symptoms of locomotor ataxia may be divided into 
three stages: (1) The stage of pain; (2) that of ataxia, and 
(3) that of paralysis. 

1. Stage of Pain .—The following are the characteristic 
symptoms of this pre-ataxic stage : 

(a) Pain , of a paroxysmal darting character, appears in 90 
per cent, of the cases. The pains are bilateral, dart down 
the legs, and are generally referred to the deeper structures 
of the limb. Their distribution is irregular, rarely corre¬ 
sponding to the nerve-trunks. The characteristics of the 
pains are their “ lightning ” character and the absence of 
local tenderness. Occasionally trophic eruptions appear. In 
rarer instances the pain may be diffused and superficial, or 
the feeling may be described as one of intense heat or cold. 
Lightning pains in the arms occur when the lesion extends 
to the cervical enlargement of the cord. Pain may be 
absent or insignificant in a few cases beginning with rapid 
optic atrophy, and in these patients ataxia is not apt to be 
developed. 

(ft) There are symptoms of perverted sensation. The 
patient may complain of numbness or tingling in the legs or 
the feet, or may feel as though he were walking on cotton 
or on air-bags instead of on solid ground. There may be a 
sensation of tightness and pressure about the waist. In some 
instances the “ muscular sense ” becomes so impaired that 
the patient cannot tell in what position the limbs are placed 
when the eyes are shut. During this first stage, however, 
the sensory symptoms are subjective, and areas of anaesthe¬ 
sia or of retarded sensation cannot be demonstrated. 

(c) Loss of knee-jerk (Westphal’s symptom) is one of the 
earliest indications of the disease, and its association with 
the lightning pains and the ocular symptoms forms a symp- 


Sl6 MANUAL OF THE PRACTICE OF MEDICINE. 


tom-group absolutely diagnostic of locomotor ataxia. The 
superficial reflexes remain good. 

(d) Ocular Symptoms .—There may be ptosis, strabismus, 
double vision, or in rare cases ophthalmoplegia externa. 
Contracted pupils (“ myosis spinalis ”) are frequent, but not 
constant. Optic atrophy may develop, causing dimness and 
restricted field of vision and color-blindness, and the atrophy 
may progress until the vision is entirely lost. Cases in 
which the atrophy of the optic nerve appears early and pro¬ 
gresses rapidly do not seem to develop the second stage of 
ataxia. The Argyll-Robertson pupil occurs during the first 
stage in over 80 per cent, of the cases. In this condition 
the pupils do not react to light, but accommodation to dis¬ 
tance is preserved. 

(e) Bladder and Rectum .—There may be lightning pains 
referred to these viscera. Constipation is usually obstinate. 
Micturition may be frequent and painful, or there may be 
imperfect control of the bladder, with dribbling, partial re¬ 
tention of urine, and cystitis. Impotence may appear, oc¬ 
casionally preceded by priapism and sexual excitement. 

2. Stage of Ataxia .—Old symptoms persist while new 
symptoms appear. The lightning pains may continue, but 
they tend to become less and less severe. Objective sensory 
disturbances can now be demonstrated ; there may be areas 
of anaesthesia or hyperaesthesia or of retarded sensation. 
The power of localizing pain may be lost, and the muscular 
sense becomes more and more impaired, so that motions 
cannot be made accurately without the aid of sight; hence 
a blind ataxic patient may become almost totally helpless. 
The eye-symptoms noted above continue, or they may 
appear for the first time. Optic atrophy occurs in 20 per 
cent, of the cases, and its antagonism to the development of 
ataxia has already been noted. There is usually difficulty 
in emptying the bladder, and retention with cystitis is apt to 


L OCOMO TOR A TAXI A. 8 1 7 

result. Deafness may occur from neuritis of the auditory 
nerve. The characteristic symptoms of the second stage are 
ataxia, visceral crises, and trophic changes. 

Ataxia usually develops in the legs, although in rare 
instances the arms may be first involved. The patient loses 
the power to co-ordinate muscular movements so as to pro¬ 
duce a harmonious result There is an inability to stand 
steadily with the eyes shut (Romberg’s symptom), to walk 
readily in the dark, or to turn quickly without falling. In¬ 
co-ordination of the arms is usually apparent in writing, in 
buttoning the clothes, or in handling the knife and fork 
when at table. Ataxia is demonstrated by having the 
patient stand or walk with the eyes shut, or touch toe to 
heel or heel to knee, or to rapidly touch the nose with the 
finger when the eyes are shut. The gait becomes character¬ 
istic. The legs are far apart; the body is inclined forward, 
so that the support of a cane may be a necessity. The foot 
is lifted high at each step, and is planted forcibly upon the 
ground with a stamp or a slap. The muscular power is 
maintained, and the nutrition of the muscles, except toward 
the close, is usually unimpaired. 

Visceral crises are characterized by paroxsymal pain in 
the various viscera. Thus, gastric, laryngeal, renal, cardiac, 
rectal, and genital crises are described, of which the gastric 
and the laryngeal are the most common, and are due to 
neuritis of the pneumogastric nerve. A gastric crisis consists 
of severe paroxysmal pain, vomiting, and hyperacidity. There 
may be haematemesis. The laryngeal crisis gives rise to 
dyspnoea, hoarse coughing, and intense pains in the shoulder 
and spine. There may be fatal asphyxia, or the larynx may 
become anaesthetic, so that death may result from aspiration- 
pneumonia. Renal crises may reproduce the symptoms of 
calculus. Cardiac crises give rise to pain in the heart, ir¬ 
regular and feeble pulse, and syncope. 

52 


8 1 8 MANUAL OF THE PRACTICE OF MEDICINE. 


Trophic Changes .—Of these changes, the most common 
are the arthropathies or joint-lesions known as “ Charcot’s 
joints” (Fig. 62), which occur in from 5 to 10 per cent, of 



Fig. 62.—Locomotor ataxia, showing Charcot’s knee (personal observation). 


all cases. These changes are most common in the larger 
joints, especially the knee. The joint swells rapidly from 
serous effusion, the articular ends of the bones become 
absorbed, ligaments soften so that dislocations and unnatural 






L OCOMO TOR A TAX/A. 


819 

mobility become evident, and there is an irregular produc¬ 
tion of new bone about the edges of the articular surfaces. 
These changes are essentially trophic in character, but an 
exciting cause may be found in some traumatism of which 
the patient is unconscious owing to the anaesthesia of the 
pai ts. The joint-lesions progress without fever and without 
pain, and the symptoms may develop in from twenty-four to 
forty-eight hours. 

The chief points of differential diagnosis from rheuma¬ 
toid arthritis are as follows : 


Rheumatoid Arthritis. 

Hypertrophy. 

Painful. 

Limited mobility. 

Slow process. 

Small joints. 

Symmetry of lesions. 

No ataxia. 


Charcot's Joint. 

Atrophy. 

Painless. 

Increased mobility. 

Rapid process. 

Large joints. 

No symmetry; usually unilateral. 
Ataxia. 


Besides Charcot’s joint other trophic changes may occur. 
The bones may rarefy and be the seat of spontaneous frac¬ 
ture. Absorption of the articular ends of the bones leads to 
dislocation. There may be herpes, oedema, local sweating, 
perforating ulcer of the foot, inflammation and falling of the 
nails, and atrophy of muscles. 

3. The stage of paralysis occurs when the patient loses 
the power of walking. Paraplegia develops from involve¬ 
ment of the lateral columns. The patient may develop 
during the second or third stage of the disease general 
paresis, melancholia, or delusional insanity. Cystitis and 
pyelo-nephritis are apt to develop. Pneumonia or bed¬ 
sores may hasten the final issue. 

Prognosis.—The course of the disease is chronic, lasting 
from twenty to forty years. Ataxia is rarely developed 
until from five to eight years after the beginning of the dis- 


820 MANUAL OF THE PRACTICE OF MEDICINE. 


ease. There have been described rare instances of acute 
ataxia in which the patient became bedridden within a few 
months. Recovery never occurs, although the disease may 
be arrested at any time, especially during the first stage, 
and may even show periods of temporary improvement. 
The disease itself seldom causes death. 

Treatment.—A quiet and regular mode of life should be 
enjoined. Alcoholic and sexual excesses should be abso¬ 
lutely interdicted. Rest in bed for several months is some¬ 
times serviceable in modifying the neuralgic pains. Spinal 
douches, tepid or cool, may be ordered daily, but extreme 
temperatures should be avoided. 

The medicinal treatment is somewhat varied, as there 
seems to be no drug capable of exerting a beneficial effect 
upon the disease to any appreciable extent. The drugs that 
have been recommended are mercury and iodide of potas¬ 
sium, especially in recent syphilitic cases; arsenic in full 
doses; nitrate of silver in gr. \ doses three times daily for 
periods of not longer than two months; chloride of sodium 
and gold; chloride of aluminum in 2- to 4-grain doses; and 
ergot in moderate doses. 

The pains may be relieved by counter-irritation to the 
spine, preferably by the thermo-cautery applied every two 
or four weeks, but the application of counter-irritants should 
not be severe, especially over anaesthetic portions of the 
skin, as destructive trophic changes may ensue. Pain may 
als'o be relieved by phenacetine or antipyrine, but opium 
should be given with caution, for fear of the habit being 
formed. 

The treatment by suspension is now being abandoned, as 
the published results do not agree with the first enthusiastic 
reports. Charcot’s joints are to be treated by rest and 
apparatus. Morphine may be indicated during the visceral 
crises. 


ATAXIC PARAPLEGIA. 


821 


HEREDITARY ATAXIA. 

Etiology and Synonym.—The disease may or may not 
be hereditary; in the latter case a history of nervous dis¬ 
orders—insanity, inebriety, or nervous irritability—is gener¬ 
ally obtained. The disease, which is apt to appear between 
the fifth and fifteenth years, rarely as late as the twentieth 
year, is one of defective development. Synonym: Fried¬ 
reich’s ataxia. 

Pathology. —There is extensive sclerosis of the posterior 
and lateral columns of the cord; this sclerosis may extend 
upwards to involve the medulla. 

Symptoms. —Ataxia is first developed in the legs, but 
the gait differs from that of locomotor ataxia in being more 
swaying and irregular and less stamping. Romberg’s symp¬ 
tom may or may not be present, and the reflexes may be 
preserved. Ataxia appears in the arms, giving rise to irreg¬ 
ular choreiform movements. Rhythmical movements may 
also be observed during rest. Nystagmus and slow, scan¬ 
ning speech are commonly observed, but visceral symptoms 
and optic atrophy are uncommon. Trophic changes are not 
observed. There is a fairly characteristic deformity of the 
foot; the patient walks on the outer edge of the foot, 
the big toe is flexed dorsally upon the first phalanx, and 
talipes equinus is developed. There are no sensory symp¬ 
toms. The mind becomes impaired late in the disease. 
As the disease progresses paralysis appears; this paralysis 
may become complete. 

Prognosis. —The disease is incurable, but its course ex¬ 
tends over years. 

Treatment is unavailing. 

ATAXIC PARAPLEGIA. 

Etiology. —Males of middle age are most frequently 
affected. There may be a history of exposure to cold or 


822 MANUAL OF THE PRACTICE OF MEDICINE. 

of sexual excesses, but antecedent syphilis is rarely to be 
demonstrated. 

Pathology.—The lesion consists of a combined sclerosis 
of the posterior and lateral columns, beginning in the lum¬ 
bar region. The nerve-roots are not involved as in loco¬ 
motor ataxia. 

Symptoms.—There are slowly developing weakness and 
rigidity of the legs, with ataxia. The knee-jerk is exag¬ 
gerated, and ankle-clonus can easily be obtained. The 
Romberg symptom is generally well marked. A dull, 
aching pain in the sacral region is the only sensory symp¬ 
tom of importance. Eye-symptoms are rare. The ataxia 
and weakness may extend to the arms, and in many cases 
there may be developed mental symptoms resembling those 
of general paresis. The muscular weakness ultimately 
merges into paralysis. 

Prognosis.—The disease is incurable. Death results 
from complications rather than from the disease itself. 

The treatment is that of chronic myelitis. 

MYELITIS, ACUTE AND CHRONIC. 

Etiology.—Myelitis may occur (i) from excessive physi¬ 
cal exertion, from exposure to wet and cold, or from sexual 
excesses; (2) from injury or disease of the vertebral bones 
causing compression or destruction of the spinal cord, or 
from tumors of the cord itself; (3) from acute infectious 
diseases, especially small-pox, measles, and typhus fever; 
(4) syphilis as an exciting or predisposing cause of myelitis 
is questionable. 

Pathology.—The affected area of the cord feels soft and 
may even be diffluent. The softened area may be grayish 
or reddish in color (“ red” or “ gray softening ”) according to 
whether or not small hemorrhages into the cord-substance 
have occurred. The nerve cells and fibres swell, undergo 


MYELITIS , ACUTE AND CHRONIC. 823 

fatty degeneration, and the myelin oozes out as fatty drop¬ 
lets. Large numbers of inflammatory corpuscles are every¬ 
where present, and “ Deiter’s spider-cells,” due to prolifera¬ 
tion of the neuroglia, are to be seen. The laminated bodies 
known as “ corpora amylacea ” are also present. The blood¬ 
vessels are dilated and may rupture. The meninges may 
also be involved. After a time conservative changes assert 
themselves. The area becomes firm from an increase of 
connective tissue, so that the cord at the affected point be¬ 
comes converted to a mass of cicatricial tissue containing 
perhaps a few nerve-fibres and cells. To this condition the 
name of “ chronic myelitis ” is applied. 

Secondary degenerations result (1) in the lateral columns 
below the lesion, and (2) in the posterior column and direct 
cerebellar tract above the lesion. 

The affected area varies. In general myelitis the cord is 
involved along its entire length; in disseminated myelitis 
various segments of the cord at different levels are affected; 
in transverse myelitis one or two segments of the cord at 
one level are destroyed. 

The effects of a transverse lesion of the cord are— 
(1) Voluntary motion is cut off from the parts below the 
lesion—paralysis. (2) Sensation is cut off from the parts 
below—anaesthesia. (3) Inhibitory fibres from the motor 
cortex checking over-reflexes are destroyed at the site of 
the lesion—increased reflexes. (4) The nutrition of the 
parts supplied directly from the affected area is impaired, 
atrophic changes resulting in nerve, muscle, and skin. 

Symptoms. —Four stages are described: (1) A stage of 
premonition, (2) one of irritation, (3) one of destruction, 
and (4) one of descending degeneration. 

1. Premonitory Stage .—There may be peculiar sensations 
in the parts afterward to be more seriously affected, and 
motor weakness may be noticed. There may be the 


824 ' manual of the practice of medicine . 

“girdle sensation ” of a string tied about the waist, from 
irritation of the nerves at the upper level of the lesion. In 
other cases these symptoms are absent, or there may be 
only a chill and fever. 

2. The irritative stage is of short duration. Sensory 
symptoms consist of hyperaesthesia and neuralgic pains 
below the lesion, and the girdle-sensation. Pain in the 
back is uncommon unless the meninges become inflamed. 
The sensory symptoms of irritation soon become admixed 
with those of destruction, and feelings of numbness and 
areas of anaesthesia appear. The motor symptoms consist 
of twitchings, cramps, and spasms, combined with some loss 
of voluntary power. The duration of this stage varies from 
several hours to one or two days. 

3. Stage of Destruction .—Two groups of symptoms are 
recognized—one, direct , due to the destruction of cord- 
tissue, and one, indirect , due to the cutting off of impulses to 
and from the brain. 

Direct symptoms are observed in the parts supplied 
directly from the affected segments. There is muscular 
paralysis, with atrophy and the reaction of degeneration. 
Reflexes are lost. There is anaesthesia of the skin supplied 
by the affected spinal nerves, with vaso-motor symptoms 
(coldness, sweating) and atrophic changes, as bed-sores. 
The atrophic bed-sores are deep and gangrenous. The 
distribution of the direct symptoms depends upon the 
extent of the lesion. In general myelitis they are universal: 
if disseminated, they are scattered; if transverse, they are 
limited to one level, the arms being involved in cervical 
myelitis, the trunk in dorsal myelitis, the legs if the myelitis 
involve the lumbar enlargement. 

Indirect symptoms result from the severance of the motor 
pyramidal and the sensory fibres at the site of the lesion. 

Below the lesion there is paralysis, with increased reflexes 


MYELITIS , ACUTE AND CHRONIC. 825 

and muscular rigidity. The paralyzed muscles do not 
atrophy, and there is no reaction of degeneration. If the 
myelitis involve the lumbar enlargement, direct symptoms 
may be present in the legs—paralysis, atrophy, loss of 
reflexes, and the reaction of degeneration. 

If the reflex centre for the bladder be destroyed, the bladder 
will no longer contract to expel its contents, but there will be 
incontinence from over-distention. Usually, however, the 
lesion is higher up than this, so that the reflex bladder- 
centre is still intact; there will then be reflex and uncon¬ 
scious passage of urine. The danger of cystitis threatens 
every case of myelitis. The functions of the rectum are 
similarly affected. 

There is regularly anaesthesia below the lesion. The imper¬ 
fect sensation allows of the formation of bed-sores, from pres¬ 
sure or from dirt, over the sacrum, the glutei, or the heels. 
These pressure bed-sores are at first superficial, and can 
be prevented by careful nursing. The atrophic bed-sores 
in areas of skin supplied by nerves from the destroyed seg¬ 
ment cannot be prevented, and they are large, deep, and 
gangrenous. 

Cerebral symptoms are rare. There may be optic neur¬ 
itis with blindness. The pulse varies from 100 to 140; the 
temperature varies between 102° and 104° F. The fever 
quickly subsides unless cystitis, pyelitis, or acute atrophic 
bed-sores develop. During this stage the patient may die 
from paralysis of the respiratory muscles, pneumonia, 
cystitis, pyelitis, suppurative nephritis, or acute atrophic 
bed-sores. The majority of patients, however, pass into 
the stage of descending degeneration, or “ chronic myelitis. 

4. Stage of Descending Degeneration .—In a few cases 
some motor power is regained and some sensations are per¬ 
ceived, so that the patient is able to get about on crutches, 
although with spastic paraplegia and loss of bladder- 


826 MANUAL OF THE PRACTICE OF MEDICINE. 


control. In other cases no improvement is noted, and the 
patient remains bedridden, with paralyzed, twitching limbs 
and cystitis. Pain in the back develops in the majority of 
cases, from the occurrence of chronic meningitis. Death 
results from suppurative nephritis, pneumonia, or bed-sores. 

Prognosis. —In very acute cases death may result in five 
or ten days. Transverse myelitis in the cervical region is 
usually fatal from paralysis of the respiratory muscles. The 
majority of cases, however, pass into the chronic condition 
of spastic paraplegia, from which but trifling improvement 
can be expected. 

Treatment.— During the earlier stages the patient should 
lie upon the side or face while the spine is cupped or is 
covered with a Chapman ice-bag. Active purgation by 
calomel or salts is indicated at the onset. Ergot in large 
doses has been recommended, but not too much is to be 
expected from its use. Morphine may be necessary for the 
relief of the pain. Great care should be exercised to 
prevent bed-sores and cystitis. The sheets should be 
drawn smooth, without wrinkles, and should be kept free 
from crumbs. The skin of the back is best hardened by 
daily frictions with alcohol and alum-water. The bed 
should also be kept dry, pads of absorbent cotton or a urinal 
being placed in position for the incontinence of the urine. 
Carefully padding the patient with small pillows may pre¬ 
vent a bed-sore, should a pressure-point become red and 
chafed, while in many cases a water-bed is indispensable. 
When bed-sores occur, simple antiseptic dressings are indi¬ 
cated. For the prevention of cystitis the urine should be 
drawn at regular intervals. The catheters should be kept 
surgically clean. If cystitis develop, the bladder should be 
washed out daily with a boric-acid solution (aj: Oj). 

For the chronic condition counter-irritation of the spine 
has been advised, but blistering agents should never be 


ACUTE ASCENDING PARALYSIS . 82 / 

used, as there is danger of bed-sores developing. Spasm 
of the limbs is relieved by heat to the spine or by general 
hot baths. Massage is indicated to keep up the nutrition 
of the muscles. Drugs are of no value in myelitis. Potas¬ 
sium iodide and mercury may be given to syphilitic subjects, 
and phosphorus and arsenic may be employed as nerve- 
tonics. Nitrate of silver (gr. is often recommended. 
Strychnine is contraindicated if spasm exist in the paralyzed 
muscles. 


ACUTE ASCENDING PARALYSIS. 

Etiology and Synonym.—The disease is most common 
in men between the ages of twenty and thirty. Some cases 
have followed infectious fevers. Synonym: Landry’s paralysis. 

Pathology.—In many of the cases an interstitial neuritis 
of the nerve-roots has been demonstrated, so that the 
disease has been classed as a peripheral neuritis. In other 
cases, however, no lesions have been found, so that it is 
supposed that the paralysis is due to some form of microbic 
poisoning. The disease bears a close resemblance to para¬ 
lytic rabies. 

Symptoms.—Weakness in the legs merges within a few 
hours into paralysis, which spreads to involve the trunk, 
arms, and neck. Finally the muscles of respiration, deglu¬ 
tition, and articulation become affected, and there may be 
facial and eye-palsies. The reflexes are lost, but the mus¬ 
cles neither waste nor show the electrical reactions of de¬ 
generation. There may be numbness, tingling, or hyperaes- 
thesia, but sensory symptoms are neither constant nor 
essential. The bladder and rectum are seldom involved. 
Febrile reaction is trifling. 

Prognosis.—Death may result within two days or may 
be postponed for one or two weeks. Recovery has occurred 
only in rare instances. 


828 MANUAL OF THE PRACTICE OF MEDICINE. 


Treatment.—Ergotin in 2-grain doses may be given 
every hour, and success has followed its administration; 
sodium salicylate and benzoate also have been recom¬ 
mended; otherwise the treatment is symptomatic. 

SYRINGOMYELIA. 

Etiology.—This rare disease is probably of congenital 
origin. Its exact cause is unknown. The symptoms 
usually appear in males between the ages of fifteen and 
twenty-five. 

Pathology.—There is a development of embryonal neur¬ 
oglia-tissue about the central canal of the spinal cord ex¬ 
tending to involve the entire central gray matter. Degen¬ 
eration and liquefaction result in the formation in the spinal 
cord of a cavity filled with cerebro-spinal fluid; the walls 
of the cavity are composed of gliomatous tissues. The 
usual situation is in the lower cervical and upper dorsal 
region. In other cases the cavity extends the entire length 
of the spinal cord. The cavity may invade the anterior 
horns, causing the symptoms of chronic anterior polio¬ 
myelitis, or may invade the posterior horns and columns, 
causing the symptoms of posterior sclerosis. 

The symptoms begin insidiously about the time of 
adolescence, and extend over years. There are aching 
pains in the neck and the arms, followed by muscular 
atrophy, first in the hands, then in the arms and trunk. 
There is a loss of the sensations of temperature and 
pain, but the touch-sensations remain intact—a form of 
partial anaesthesia which is almost pathognomonic. The 
legs become involved late in the disease, and show the 
symptoms of spastic paraplegia. From the involvement of 
the spinal muscles, curvature (scoliosis) almost regularly 
results. Vaso-motor, secretory, and trophic symptoms are 
common in the affected parts—cyanosis, oedema, sweating, 


C OAIPRE SS / ON- M YE LITIS . 


829 


ulcers, bullae, defective growth of the nails, brittleness of 
the bones. Felons are common. There is loss of control 
over the bladder and rectum if the lumbar region of the 
cord be involved. 

The prognosis is bad, although the disease extends over 
years. The latter stages of the disease resemble chronic 
muscular atrophy. Death may result from involvement of 
the medulla. 

Treatment is inoperative. Arsenic and nitrate of silver 
are generally given as a routine, but beneficial results are 
not to be expected from medication. 

COMPRESSION-MYELITIS (SLOW COMPRESSION 

OF THE CORD). 

Etiology. —The spinal cord may be compressed (a) by 
disease of the vertebral bones, especially caries; ( b ) by 
thickened membranes; (c) by tumors of the cord, mem¬ 
branes, or bones. The most common tumors are carcinoma, 
(usually secondary to primary growths in the breast), retro¬ 
peritoneal sarcoma and aneurysm (causing erosion of the 
bodies of the vertebrae, so that they come to lie directly on 
the spinal cord itself), and sarcoma of the membranes. 

The pathology is that of a pressure-atrophy. 

The symptoms are those of chronic myelitis slowly 
developing with a prolonged stage of irritation. 

Compression of the spinal-nerve-roots causes neuralgic 
pains with areas of anaesthesia (“ anaesthesia dolorosa ”) and 
with muscular spasms followed by paralysis, loss of reflexes, 
and atrophy of muscle. 

Compression on a spinal segment gives rise to anaesthesia, 
paralysis, atrophy, loss of reflexes, and the reaction of de¬ 
generation in the muscles supplied directly from the com¬ 
pressed segment. Below the affected segment there are the 
symptoms of spastic paraplegia—paralysis, increased re- 


830 MANUAL OF THE PRACTICE OF MEDICINE . 

flexes, absence of atrophy and of the reaction of degenera¬ 
tion. There is loss of bladder- and rectum-control. If the 
compressed segment be in the lower dorsal and lumbar 
regions, the reflexes in the legs will be lost and the muscles 
will atrophy. 

The prognosis depends upon the cause of the compression. 

Treatment is that of the original cause. Caries of the 
vertebrae is best treated by suspension. Tumors may be 
removed by operation if it be practicable. In some cases 
of bone disease laminectomy may be performed with 
benefit. 


TUMORS OF THE SPINAL CORD. 

Etiology and Pathology.—Tumors of the spinal cord are 
rare and are usually secondary to growths elsewhere. Sar¬ 
coma and tubercular, syphilitic, and gliomatous growths are 
most frequently observed. The compression of the spinal 
cord leads to a chronic myelitis at the seat of the growth, 
and in rare cases may induce the condition of syringo¬ 
myelia. 

Symptoms.—The symptoms are those of a compression- 
myelitis or of Brown-Sequard’s paralysis, of slow develop¬ 
ment and characterized by such extreme pain in the sensory 
areas corresponding to the segment in which the tumor 
grows that the name “paraplegia dolorosa” has frequently 
been applied. 

The prognosis is bad in inoperable growths. 

The treatment is to remove the tumor if possible; other¬ 
wise the treatment is symptomatic. 

BROWN-SEQUARD’S PARALYSIS. 

Etiology.—One half of the spinal cord may be destroyed 
by tumors, by hemorrhages, by disease of the vertebral 
bones, or by traumatism. 


DISEASES OF THE OPTIC NERVE. 831 

The pathology is that of a destructive lesion involving 
a lateral half of a spinal segment. 

The symptoms are best appreciated by consulting the 
following table of Gowers: 


Cord. 


Zone of cutaneous hyperaesthesia. 
Zone of cutaneous anaesthesia. 

Lesion. 



Motor palsy. 

Hyperaesthesia of skin. 
Muscular sense impaired. 
Reflex action at first lessened, 
then increased. 

Temperature raised. 


Muscular power normal. 

Loss of sensibility of skin. 
Muscular sense normal. 

Reflex action normal. 

Temperature same as that above 
the lesion. 


Treatment is directed to the cause of the hemi-lesion; 
otherwise the treatment is that of myelitis. 


5. DISEASES OF THE CRANIAL NERVES. 

OLFACTORY NERVE. 

Anosmia, or loss of the sense of smell, may occur with 
chronic nasal catarrh or with diseases of the olfactory 
nerves or bulbs following meningitis, frontal tumors, or 
caries of the bones. The symptom is not uncommon 
among insane and hysterical patients. 

Hyperosmia, or increased sensitiveness, and parosmia, or 
subjective perversions, of the sense of smell, are not infre¬ 
quently observed in neurotic patients. Parosmia may pre¬ 
cede an attack of epilepsy. 

OPTIC NERVE. 

Many of the diseases of the optic nerve clearly belong 
to the domain of ophthalmology, and therefore will not be 
considered here. 













832 MANUAL OF THE PRACTICE OF MEDICINE. 


Destructive lesions in various parts of the optic tract 
produce the following results (see Fig. 55 ): 

1. Lesions of the optic nerve produce blindness of the 
corresponding eye. 

2. Lesions of the chiasm may produce blindness of both 
eyes (if the chiasm be totally destroyed), temporal hemiano- 
pia (if the central part of the chiasm be involved), or nasal 
hemianopia (if both lateral regions of the chiasm be affected). 

3. Lesions of the optic tract produce lateral hemianopia. 

4. Lesions of the cuneus produce lateral hemianopia. 

5. Lesions of the angular gyrus give rise to hemianopia 
and mind-blindness, rarely to crossed amblyopia. 

Hemianopia, though usually of organic origin, may occur 
with hysteria, migraine, and lithaemia. In hemianopia, if 
the pupil reacts when a ray of light is thrown upon the 
sensitive half of the retina, the lesion is in the optic radia¬ 
tion or in the cerebral cortex. 

THIRD NERVE. 

Nuclear lesions of the third nerve are usually associated 
with disease of the other ocular-nerve-centres (see Oph¬ 
thalmoplegia). Disease of the third-nerve-trunk is not 
uncommon. The nerve may be the seat of a neuritis (espe¬ 
cially with locomotor ataxia and after diphtheria), it may be 
compressed by meningitis, tumors, or aneurysms at the base 
of the brain, or it may be paralyzed from exposure to cold, 
from rheumatism, from syphilis, or by an attack of mi¬ 
graine. Paralysis of the third nerve gives rise to external 
strabismus, ptosis, dilatation of the pupil, loss of pupil-reflex 
and of accommodation to distance, and to diplopia, or 
double vision. 

A form of oculo-motor palsy is described as occurring 
chiefly in women, and as recurring at intervals of several 
months, associated with pain and migraine. 


DISEASES OF THE FIFTH NERVE. 


8 33 


Spasm of the muscles supplied by the third nerve is not 
uncommon in meningitis and in hysteria. Slow rhythmical 
oscillations of both eyeballs (nystagmus) occur in congenital 
and acquired brain affections and in albinism, and is not 
uncommon among coal-miners. 

FOURTH NERVE. 

The causes of fourth-nerve-paralysis are similar to those 
causing third-nerve-palsy. The symptoms are a slight con¬ 
vergent strabismus when the eye is rolled downward, and 
double vision when the patient looks down. 

FIFTH NERVE. 

Paralysis. —The nucleus may be involved by hemor¬ 
rhages or tumors of the pons, or the branches of the nerve 
may be affected within the cranium by meningitis, caries, 
or tumors. The lower divisions are not infrequently in¬ 
volved by tumors of the upper jaw. Primary neuritis is 
rare. 

Symptoms. — Sensory .—There is anaesthesia of the skin 
of the face and head, the conjunctiva, and the mucosa of the 
lips, tongue, soft and hard palate, and nose. The anaesthe¬ 
sia may be preceded by hyperaesthesia or by tingling feel¬ 
ings. 

Motor .—The temporal and masseter muscles are paralyzed, 
and the jaw, when depressed, moves toward the paralyzed 
side. The motor palsy is usually due to lesions involving 
the trunk of the nerves. 

Trophic and Vaso-motor Changes .—There may be ulcera¬ 
tions of the mucosa, falling of the teeth, opacity and ulcera¬ 
tion of the cornea, diminished salivary, nasal, buccal, and 
lachrymal secretions, flushings and pallor, and herpes. The 
trophic changes occur if the Gasserian ganglion is affected. 

53 


834 MANUAL OF THE PRACTICE OF MEDICINE . 

Gustatory. —There is regularly loss of the sense of taste 
in the anterior two-thirds of the tongue. 

Spasm of the Muscles of Mastication (Trismus; Lock¬ 
jaw).—Trismus occurs with tetanus, tetany, and hysteria, 
from reflex irritation from diseases of the teeth and jaws, 
and from irritation of the motor nucleus of the fifth nerve. 
Trismus nascentium is caused by infection through the um¬ 
bilicus of newly-born children. The spasm may be tonic or 
clonic. Clonic spasms may occur as a symptom of chorea. 

Neuralgia (Tic Douloureux).—Neuralgia of all the 
branches of the fifth nerve is rare; usually the ophthalmic, 
alone or with the superior maxillary division, is affected. 

For the etiology of neuralgia see the article on Neuralgia. 

Supraorbital neuralgia is marked by shooting pains 
along the course of the nerves, by painful spots at the 
supraorbital notch, at the inner angle of the orbit, and at 
the junction of the bone and cartilage of the nose. There 
are usually intolerance to light, injection of the conjunctiva, 
and increased lachrymation. The skin may be exquisitely 
tender to the touch. In severe cases there may be painful 
spasm of the facial muscles (spasmodic tic). In protracted 
cases the hair on the affected side may become gray. 

Superior Maxillary Neuralgia. —Pain is referred to the 
teeth of the upper jaw, and a painful point is located at the 
infraorbital foramen. 

Inferior Maxillary Neuralgia. —The pain is experienced 
about the ear and in the teeth of the lower jaw, and painful 
spots may be elicited along the auriculo-temporal nerve. 

The treatment of neuralgia will be considered under a 
separate heading (see page 859). 

SIXTH NERVE. 

Abducens palsy occurs most commonly with syphilis and 
locomotor ataxia, and causes convergent strabismus, double 



DISEASES OF THE SEVENTH NERVE. 


S35 

vision, and inability to rotate the eye outward. When the 
nucleus of the nerve is involved, there is, in addition to the 
paralysis of the external rectus, an inability of the internal 
rectus of the unaffected eye to turn that eye inward. Both 
eyes are therefore deviated to the opposite side, away from 
the lesion (conjugate deviation). 

SEVENTH NERVE—FACIAL. 

Facial Paralysis (Bell’s Palsy).—The innervating fibres 
of the facial muscles may be paralyzed (1) above the 
nucleus, (2) at the nucleus, or (3) after leaving the nucleus. 

1. Supranuclear paralysis is caused by destructive lesions 
of the cortex, corona radiata, and internal capsule, and is, 
as a rule, accompanied by hemiplegia on the same side as 
the facial paralysis. Facial paralysis alone from cortical or 
central lesions is uncommon. Supranuclear paralysis differs 
from the peripheral form in that the electrical reactions of 
the affected muscles remain normal, and the upper branches 
of the facial nerve are not involved, so that the patient can 
wink and can corrugate the forehead. 

2. Nuclear paralysis is uncommon. The nucleus may be 
involved by tumors, by hemorrhages, or by softening, or 
with diphtheria or anterior poliomyelitis. The symptoms 
are the same as those of the peripheral type. Lesions of 
the pons may cause facial paralysis on the same side, and 
crossed hemiplegia, the so-called “ crossed facial paralysis ” 
(See Fig. 57). 

3. Peripheral or Infranuclear Paralysis .—The nerve-trunk 
may be involved (a) within the pons, by hemorrhage, tumor, 
or softening, with the production of crossed facial paralysis; 
(b) at its point of emergence, by tumors, meningitis, syphilis, 
or fractures at the base of the skull; (c) in the Fallopian 
canal, by diseases of the middle ear or by caries of the 
petrous portion of the temporal bone; (d) at its emergence 


836 MANUAL OF THE PRACTICE OF MEDICINE. 


through the styloid foramen, by blows, cuts, tumors of the 
parotid gland, or by the pressure of the forceps in instru¬ 
mental delivery; (e) exposure to cold is a frequent cause 
leading to a mild form of neuritis. 

Symptoms.—In peripheral facial paralysis all the 
branches of the nerve are usually affected. The expression 
of the face is striking and characteristic. The paralyzed 

half of the face is lax, 
wrinkles are obliterated, 
and the naso-labial fold 
is no longer evident. 
The lower lid droops, 
the eye waters, and the 
eye cannot be closed 
voluntarily. The corner 
of the mouth sags, the 
mouth is drawn away 
from the affected side, 
and there is constant 
drooling of saliva. Mas¬ 
tication and articulation 
become impaired. 

In many cases there is 
said to be a paralysis of 

Fig. 63._Sch em »ti c repr« Se Mation of the mmk the soft pa ] ate b Ut t hj s 
of the facial from the base of the skull to the pes 1 

anserinus; different localizations of the lesion in is doubted by GoWd'S. 
paralysis (Strumpell): N.f, facial nerve; N.p.s, 
great superficial petrosal; N.c.c.p.t, nerve com¬ 
municating with the tympanic plexus ; N st, 
stapedius; Ch.t, chorda tympani ; G/., fibres of 
taste; S.p.s, nerve governing the secretion of 
saliva; N.a, acoustic nerve; G.g, geniculate 
ganglion; F.st, stylo-mastoid foramen; N.a.p, 
posterior auricular nerve. 

calization of the lesion 
can readily be appreciated by an examination of the accom¬ 
panying diagram (Fig. 63). 



Facial paralysis is ren¬ 
dered evident by any at¬ 
tempt at talking, whist¬ 
ling, or inflating the 
cheeks. The exact lo- 







DISEASES OE THE SEVENTH NERVE . 837 

1. Paralysis of facial muscles; taste, secretion of saliva, 
and hearing are normal; the seat of the affection is in the 
portion between 1 and 2, usually in the trunk of the facial 
nerve, below the Fallopian canal. 

2. Paralysis of the facial muscles, disturbance of taste, and 
eventually diminished secretion of saliva; hearing normal; 
the seat of the lesion is in the Fallopian canal, between 2 
and 3. 

3. Paralysis of the facial muscles, disturbance of taste, 
diminished secretion of saliva, abnormal acuteness of hear¬ 
ing ; the seat of the lesion is between 3 and 4. 

4. Paralysis of the facial muscles, disturbance of taste, 
diminished secretion of saliva, abnormal acuteness of hear¬ 
ing, and paresis of the soft palate (?); the seat of the lesion 
is in the geniculate ganglion, between 4 and 5. 

5. Paralysis of the facial muscles, diminished secretion 
of saliva, abnormal acuteness of hearing, paresis of soft 
palate (?), but no disturbance of taste; the seat of the lesion 
is above the geniculate ganglion, between 5 and 6. 

Erb distinguishes three grades of severity of facial 
paralysis: 

1. Mild Form. —This form usually occurs after exposure 
to cold. The facial muscles are alone involved, there being 
no acuteness of hearing nor disturbance of taste. Elec¬ 
trical reactions remain good, and recovery follows after two 
or three weeks. 

2. Middle Form .—There is a partial reaction of degenera¬ 
tion. The electrical excitability of the nerve is diminished, 
but not entirely lost. In two or three weeks the A. C. C. 
is found greater than the C. C. C., and the muscles react 
slowly to the galvanic current. Recovery ensues in from 
four to eight weeks. 

3. Severe Form. —There is loss of faradic and galvanic 
excitability of the nerves; the galvanic excitability of the 


838 MANUAL OF THE PRACTICE OF MEDICINE. 

muscles shows decided reaction of degeneration. Recovery 
does not occur before eight to fifteen months. 

The prognosis of facial paralysis is usually good. In 
cases following traumatism, however, the damage done to 
the nerve may be permanent. In some cases, during con¬ 
valescence, contractures are observed in the affected muscles, 
so that the wrinkles and folds of the skin may actually be 
deepened upon the affected side. 

Spasm of the facial nerve is rare as the result of 
irritation of its nucleus. Usually spasm occurs as a habit 
in children or is due to reflex irritation. Tonic spasm may 
follow paralysis or may be due to catching cold. Facial 
spasm may be part of the affection known as “ tic convulsif,” 
characterized by spasms of various facial muscles and by 
explosive utterances, frequently of bad language. 

AUDITORY NERVE. 

The centre for hearing is in the first temporal convolution. 
Left-sided lesions in this location give rise to word-deafness. 
The fibres passing from the cortical centre to the auditory 
nucleus in the medulla may be destroyed by tumors of the 
corpora quadrigemina. 

Nuclear degeneration is uncommon. The nerve itself 
may be compressed by meningitis or by tumors or fractures 
of the base of the skull. Neuritis may complicate loco¬ 
motor ataxia, and is not uncommon with epidemic cerebro¬ 
spinal meningitis, many cases of deaf-mutism following this 
latter disease. The labyrinthine branches may be involved 
by inflammation extending from the middle ear, by over¬ 
dosing by quinine and the salicylates, and by the constant 
noises and jarring to which locomotive-makers and boiler¬ 
makers are subject. 

Destructive lesions in the course of the auditory tract 
give rise to “ nervous deafness,” frequently associated with 


DISEASES OF THE AUDITORY NERVE. 839 

tinnitus and vertigo. Sudden complete deafness is charac¬ 
teristic of syphilitic disease of the internal ear. 

The diagnosis of nervous deafness from that produced 
by local disease of the middle ear is made by the use of 
the tuning-fork. If the vibrations of the tuning-fork are 
audible when the base of the instrument is placed against 
the temporal bone, nervous deafness may be excluded. 

Meniere’s Disease (Auditory Vertigo; Labyrinthine 
Vertigo).—At the present date all cases of aural vertigo 
are spoken of as instances of Meniere’s disease, but more 
properly the name should be restricted to those cases with 
a sudden onset and recurring as a paroxysmal affection, 
originally described by Meniere in 1861. 

Etiology. —The condition is most common in males after 
the fortieth year, and appears to bear no relation to middle- 
ear disease. 

Pathology. —Whether the lesion be in the semicircular 
canals or in the cerebral centres is not known. 

Symptoms. —The patient suddenly becomes giddy; 
surrounding objects seem to revolve, or the patient himself 
may seem to be gyrating, usually from the left to the right. 
The vertigo may render walking, or even standing, impos¬ 
sible. The onset may be so abrupt that the patient will 
fall, and may even lose consciousness for a short time. 
In a few minutes the dizziness passes away; the patient is 
left pale, prostrated, and bathed with a clammy sweat, and 
nausea and vomiting are apt to follow the attack. There is 
usually deafness in one ear, never complete. 

The paroxysms recur at irregular intervals, and the 
prognosis is uncertain. Recovery occurs in some cases, 
while in others the attacks become more frequent and deaf¬ 
ness may become complete. 

Treatment. —Quinine in 20-grain doses daily for several 
weeks has been recommended by Charcot. Hypodermic 


840 MANUAL OF THE PRACTICE OF MEDICINE. 

injections of from 5 to 10 drops of a 2 per cent, solution 
of pilocarpine every second day are often of service, but 
the treatment should be restricted to robust patients. 
Nitroglycerin may be given if there be high arterial tension. 
Sodium bromide or hydrobromic acid is often of great 
service. Sodium salicylate in 5-grain doses three times 
daily is recommended by Gowers. 

GLOSSO-PHARYNGEAL NERVE. 

Nuclear degeneration gives rise to the pharyngeal symp¬ 
toms of bulbar paralysis. The nerve-trunk may be in¬ 
volved by meningitis, or may be the seat of a diphtheritic 
neuritis, causing difficulty in swallowing and loss of sensa¬ 
tion in the palate. Lesions of the root of the glosso¬ 
pharyngeal nerve do not give rise to loss of taste in the 
posterior third of the tongue, as the taste-fibres come 
originally from the fifth nerve. 

PNEUMOGASTRIC NERVE. 

The vagus gives branches to the pharynx, larynx, lungs, 
heart, oesophagus, and stomach, and is the chief afferent 
nerve of the vaso-motor centre. The nucleus may be in¬ 
volved by hemorrhage, tumor, softening, or by slow degen¬ 
eration as in bulbar paralysis. The nerve-root within the 
cranium may be compressed by meningitis, by tumors, or 
by aneurysm of the vertebral artery. In the neck the 
vagus may be injured by wounds or maybe accidentally cut 
or ligated in surgical operations. The recurrent laryngeal 
branches are frequently stretched by the growth of aortic 

or innominate aneurysms. Neuritis of the vagus is uncom¬ 
mon. 

1. Pharyngeal Branches. —Motor branches from the 
pneumogastric combine with those from the glosso-pharyn- 
geal to form the pharyngeal plexus. Paralysis may result 




DISEASES OF THE PNEUM0GASTR1C NERVE. 84 1 


from bulbar degeneration or as the result of a post-diph¬ 
theritic neuritis. I he symptom is difficulty in swallowing, 
hood may enter the larynx or may be regurgitated through 
the nose it the soft palate also be paralyzed. 

Spasm is usually a neurosis, affecting nervous people. 
Its type is the “ globus hystericus.” Spasm is one of the 
principal symptoms of hydrophobia and of pseudo-rabies. 

2. Laryngeal Branches. —The superior laryngeal branch 
supplies the mucous membrane of the larynx above the 
vocal cords, and the crico-thyroid muscle. The recurrent 
laryngeal, arising in the upper part of the thorax, supplies 
the mucous membrane below the vocal cords, and all the 
muscles except the epiglottidean and the crico-thyroid. 
The motor fibres are derived originally from the spinal 
accessory. 

The following chief forms of laryngeal paralysis are thus 
tabulated by Gowers: 


Symptoms. 

No voice ; no cough ; stridor 
only on deep inspiration. 

Voice low-pitched and 
hoarse; no cough ; stridor 
absent or slight on deep breath¬ 
ing. 

Voice little changed; cough 
normal; inspiration difficult and 
long, with loud stridor. 

Symptoms inconclusive; little 
affection of cough or voice. 

No voice ; perfect cough ; no 
stridor or dyspnoea. 


Signs. 

Both cords moderately ab¬ 
ducted and motionless. 

One cord moderately abduct¬ 
ed and motionless, the other 
moving freely, and even beyond 
the middle line in phonation. 

Both cords near together, and 
during inspiration not separ¬ 
ated, but even drawn together. 

One cord near the middle 
line, not moving during inspi¬ 
ration; the other cord normal. 

Cords normal in position and 
moving normally in respiration, 
but not brought together on an 
attempt at phonation. 


Lesion. 

Total bilateral palsy. 
Total unilateral palsy. 


Total abductor palsy. 


Unilateral abductor 
paralysis. 

Adductor palsy. 


The laryngeal palsies may be due to nuclear disease (as 
bulbar paralysis), to lesions of the trunk of the vagus or 
of the recurrent laryngeal nerves, to severe laryngeal 
catarrhs, or to over-use of the voice, or they may appear as 


842 MANUAL OF THE PRACTICE OF MEDICINE . 


hysterical conditions. For a more detailed description 
of the laryngeal palsies the reader is referred to specialized 
works upon the subject. 



Fig. 64— a, Adductor paralysis of both cords; b, adductor paralysis of left cord; c, 


abductor paralysis of both cords (Brown). 

Spasm of the laryngeal muscles may occur in children 
(see Laryngismus Stridulus and Spasmodic Croup), or in 
adults as a laryngeal crisis of locomotor ataxia. Paroxysmal 
attacks of laryngeal spasm sometimes occur in adults, usually 
in the night; they have been known to replace migraine. 
Spasm may also be induced by irritation of the recurrent 
laryngeal nerve by the pressure on it of aneurysms or 
tumors, the spasmodic dyspnoea thus induced being relieved 
by whiffs of chloroform, while the obstructive dyspnoea of 
aneurysmal pressure on the trachea or of paralytic dyspnoea 
remains unchanged. Laryngeal spasm may occur with 
tetany or hysteria. A rare condition of functional spasm 
occurs when attempts are made to speak, the cords being 
brought together too forcibly. 

3. Pulmonary Branches. —The spasmodic contraction of 
the muscular fibres of the bronchial walls in asthma is 
thought to be induced by a neurosis of the vagus. De¬ 
structive lesions of the nucleus of the pneumogastric, as 
hemorrhage or softening, are followed by rapid congestion 
of the lung, with extravasation of blood into the pulmonary 
tissue. 


DISEASES OF THE PNE UMO GAS TRIG HEP PE. 843 


4. Cardiac branches are motor, sensory, and trophic in 
character. 

(a) Motor .—Irritation of the vagus causes an inhibitory 
slowness of the heart’s action. Bradycardia may thus 
follow irritation of the vagus-nucleus or compression of the 
nerve in the neck by tumors, or the slowing of the pulse 
may be an evidence of a pure neurosis of the nerve. 
Paralysis of the vagus abolishes inhibitory action and 
allows the accelerators full sway. Tachycardia may thus 
occur with diphtheritic neuritis, wounds or accidental liga¬ 
ture of the vagus, or the involvement of the nerve-trunk 
by tumors or by toxaemic conditions depressing the activity 
of the vagus-nucleus. 

( b ) Sensory .—The vagus is the afferent nerve of the heart, 
and through it the unpleasant sensations of palpitation and 
pain are conveyed to the brain. The relation of the pneu- 
mogastric nerve to angina pectoris is not thoroughly 
understood. 

(e) Trophic .—After injury of the vagus the heart is 
usually found in the condition of acute fatty degeneration. 

5. CEsophageal Branches. —Paralysis of the oesophagus 
gives rise to difficulty in swallowing, simulating stricture. 
Spasm of the oesophagus is more frequent than paralysis. 

6. Gastric branches are sensory and motor. 

(a) Sensory branches may be the seat of pain, either from 
irritation of the terminal fibres or from spontaneous neural¬ 
gia. Hunger is generally believed to be a pneumogastric 
sensation, and it is probable that many cases of nervous 
dyspepsia are dependent upon deranged functional activity 
of the vagus nerve. 

o 

(b) Motor .—After section of the nerve, contraction-power 
of the stomach is lessened but not altogether lost. The 
cerebral vomiting of meningitis and of other brain diseases 
is due to irritation of the vagus-nucleus, and paroxysmal 


844 MANUAL OF THE PRACTICE OF MEDICINE. 

vomiting may be due to an intermitting pressure on the 
pneumogastric nerve in the neck. 

7. Intestinal branches accelerate the action of the intes¬ 
tines, but intestinal symptoms from diseases of the nerve or 
of its nucleus are exceedingly rare. 

SPINAL ACCESSORY NERVE. 

The “ accessory ” portion, arising from the medulla, joins 
the pneumogastric and supplies the laryngeal muscles. 
The “spinal” portion, arising from the cervical portion of 
the cord, supplies the sterno-mastoid and the portion of the 
trapezius muscle between the occipital bone and the acro¬ 
mion. The nucleus in the medulla may be involved in 
bulbar paralysis; the nerve-trunk may be implicated by 
meningitis, tumors, or caries. The symptoms of nuclear 
disease are those of the various laryngeal palsies. Disease 
of the spinal portion is followed by paralysis of the sterno- 
mastoid and of the upper portion of the trapezius. There is 
an absence of the normal prominence of the sterno-mastoid 
muscle in the neck, and the head is rotated with difficulty 
to the opposite side. The head may be held obliquely, but 
purely paralytic torticollis does not occur. The paralysis of 
the upper portion of the trapezius gives a concave contour 
to the neck, especially marked on deep inspiration; the 
shoulder falls a little, the scapula recedes from the spine, 
and the angle is rotated inward from the unopposed action 
of the rhomboids and the levator anguli scapulae. Eleva¬ 
tion of the arm is also impaired, as the deltoid loses some 
of the support from which it acts. Bilateral paralysis may 
occur with progressive muscular atrophy, and is not uncom¬ 
mon in children in consequence of chronic meningitis about 
the foramen magnum damaging both spinal accessory 
nerves. If both sterno-mastoids are affected, the head falls 
backward ; if both trapezii.the chin sinks upon the sternum. 







DISEASES OF THE SPINAL ACCESSORY NERVE. 845 

Spasm of the Spinal Accessory Nerve (Torticollis; 
Wry-neck).— 1. The congenital form (fixed wry-neck) affects 
the right side almost exclusively. The sterno-mastoid is 
shortened, frequently is atrophied, and usually is hard and 
firm. In some of the cases the condition is thought to 
depend upon injury to the muscle from traction upon the 
neck during birth. The muscle stands out prominently; 
the head deviates and cannot be turned toward the side on 
which the muscle is contracted. The symptoms are rarely 
noticed during early childhood, because of the shortness of 
the neck. In many cases there is an associated facial 
asymmetry, which by some is thought to be an essential 
feature of the congenital form. Congenital torticollis is of 
slight importance, as it can readily be cured by tenotomy. 

2. Spasmodic torticollis may be either clonic or tonic, 
the two varieties being frequently combined. The condition 
seems to be more frequent in males, usually between thirty 
and fifty years of age; most cases occurring in females 
under the age of thirty are of a hysterical nature. There is 
frequently a neurotic family history, but in the majority of 
cases no exciting cause can be demonstrated. 

Symptoms. —Spasm may be the first symptom, but in 
many cases there is a preceding pain of a sharp neuralgic 
or a dull character, or a sense of stiffness may antedate the 
spasm. The spasm usually comes on gradually, and may 
involve the sterno-mastoid alone, or there may be an 
associated spasm of the upper portion of the trapezius on 
the same side, or of the splenius, usually upon the opposite 
side. The scaleni and platysma myoides occasionally con¬ 
tract, or more rarely the deep cervical muscles. Bilateral 
contraction of the sterno-mastoid muscles causes a back¬ 
ward movement of the head, so that the face may look up¬ 
ward (retrocollic spasm), and there is an associated spasm 
of the frontales muscles. The various other deformities 


846 MANUAL OF THE PRACTICE OF MEDICINE. 

may be inferred by a knowledge of the anatomy of the 
affected muscles. Clonic spasms may recur every few 
minutes, are usually associated with considerable pain, and 
in time the muscles become hypertrophied. The clonic 
spasms cease during sleep and are aggravated by emotion, 
excitement, or fatigue. In some cases the spasms spread 
to the muscles of mastication, of the face, or of the arms. 

Prognosis. —The course of the disease varies. After a 
few years the disease ceases to progress and may either 
remain stationary or improve. Recurrences are common. 
The disease is usually regarded as a functional neurosis. 

Treatment.—The spasm may be relieved by valerianate 
of zinc, by asafoetida, or by sodium bromide. Chloral and 
cannabis indica are frequently of service. Hypodermic 
injections of morphine constitute the most curative mode of 
treatment, but from the long continuance of the treatment 
the habit is regularly formed, so that the treatment should 
not be inaugurated. Galvanism should be tried. In obsti¬ 
nate cases nerve-stretching, division, and excision may be 
performed. 

HYPOGLOSSAL NERVE. 

Nuclear disease is usually degenerative in character, 
forms part of bulbar paralysis, and may occur with loco¬ 
motor ataxia or from acute softening from obstruction of 
the blood-vessels. The symptoms are usually bilateral. 

Supranuclear disease may occur anywhere in the motor 
tract between the nucleus and the lowest portion of the as¬ 
cending frontal convolution. Paralysis of the tongue occurs 
upon the opposite side, and is usually associated with hemi¬ 
plegia. In supranuclear disease the tongue does not waste. 

In infranuclear disease the fibres of the nerve may be 
involved by tumor or meningitis, or the nerve may be com¬ 
pressed within its foramen by caries of the bones. There 
may be a neuritis of rheumatic or saturnine origin. In 


NEURITIS. 847 

nuclear and infranuclear disease the tongue wastes and the 

o 

reaction of degeneration is present. 

Symptoms.—In unilateral paralysis the tongue, when 
protruded, deviates to the paralyzed side; in bilateral palsy 
it lies motionless and cannot be protruded. Articulation 
and mastication are interfered with in proportion to the ex¬ 
tent of the paralysis. Sensation and taste are not impaired. 
If the hypoglossal fibres be involved within the nucleus 
or after leaving the nucleus, there may be paralysis of the 
tongue on the same side, with opposite hemiplegia (Fig. 57). 

Spasm of the tongue may be part of a general spasm, 
such as epilepsy or chorea ; the affection occurs in some 
forms of stuttering. The tongue is a not infrequent seat 
of spasm in hysteria. Spasm of the tongue may also be 
induced by reflex irritation of the fifth nerve. 

A rare form of paroxysmal clonic spasm is described, in 
which the tongue is protruded as many as forty or fifty 
times a minute. Spasm of the tongue is almost regularly 
dependent upon functional states of the nervous system that 
are removable by tonic treatment. 


6. DISEASES OF THE PERIPHERAL NERVES. 

NEURITIS. 

Neuritis may be localized in one nerve or may involve a 
number of nerves. For convenience, therefore, a localized 
and a general or multiple form are described. 

Localized Neuritis. 

Etiology.—Traumatism is the most frequent cause for a 
localized neuritis, the nerve being injured by wounds, con¬ 
tusions, fractures and dislocations of bones, sudden violent 
muscular exertion, by hypodermic injections of irritants 



848 MANUAL OF THE PRACTICE OF MEDICINE. 

such as ether, and by the steady strain on certain muscles, 
as in professional palsies. The nerve may be involved by 
an extension of inflammation from other parts, especially 
from bone disease. A nerve-trunk may also be involved by 
the growth of tumors. Cold is a not infrequent cause of 
neuritis, the facial and sciatic nerves being most commonly 
affected from this cause. This form is often spoken of as 
“ rheumatic neuritis.” The various toxic agents to be con¬ 
sidered under Multiple Neuritis may act upon a single nerve. 

Pathology.—An interstitial and a parenchymatous neur¬ 
itis occur. 

Interstitial Neuritis .—The inflammation may involve the 
perineurium or may extend into the deeper portions. The 
connective tissue becomes congested and infiltrated by 
leucocytes. The nuclei of the sheath of Schwann are 
increased, and the myelin becomes broken up into frag¬ 
ments. The axis-cylinder may ultimately develop degen¬ 
erative atrophy, so that in the final stages the nerve is rep¬ 
resented by a strand of very fatty connective tissue (the 
“ lipomatous neuritis ” of Leyden). Interstitial neuritis is the 
form which usually occurs from extension of inflammation 
from carious bone. 

Parenchymatous Neuritis .—Congestion and exudation oc¬ 
cur in the nerve-trunk, and there is a degeneration of 
individual nerve-fibres. The myelin-sheath becomes dis¬ 
integrated into fatty granules; the nuclei of the sheath of 
Schwann multiply. In severe cases the axis-cylinder also 
undergoes fatty disintegration. The products of degeneration 
liquefy and are absorbed, leaving only the collapsed sheath 
of Schwann. In this form, which resembles the secondary 
degeneration occurring in a nerve divided from its trophic 
centre, the interstitial connective tissue is but slightly 
affected. The muscles supplied by the degenerated nerve 
undergo marked atrophic changes. This form occurs in 


NEURITIS. 


849 


traumatic cases. Regeneration occurs by the growth of 
new fibres outward into the affected districts of the nerve. 

The two forms are frequently combined in non-traumatic 
cases. 



Fig. 65.—Normal nerve-fibre (Starr): a, axis-cylinder; medullary sheath; c, sheath of 
Schwann ; d, node of Ranvier ; e, incisure of Schmidt; /, nucleus of sheath of Schwann. 



Fig. 66.—Degeneration of nerve-fibres in various stages (Starr). 


Symptoms. —There is weakness or paralysis of the 
muscles to which the nerve-fibres are distributed ; motion 
is painful, and there may be at the onset twitchings or con¬ 
tractions. Atrophy of the muscles ultimately develops; 
there is loss of the faradic irritability, and the reaction of 
degeneration develops. Pain, of a boring or stabbing cha¬ 
racter, is felt along the course of the nerve and in its area 
of distribution, followed by numbness or anaesthesia. Loss 
of tactile sensation frequently occurs even if the pain be 
marked. Tenderness along the course of the nerve-trunk 
usually persists. Trophic changes may become evident: 
the skin becomes glossy or reddened and cedematous; the 
nails become defective; and there may be herpes, increased 
surface temperature, localized sweatings, and effusion into 
the joints. A localized neuritis may in rare instances 
extend upward along the larger nerve-trunks (ascending or 
migrative neuritis), and may even reach the spinal cord, 
causing a subacute myelitis. 

54 




























850 MANUAL OF THE PRACTICE OF MEDICINE. 


Prognosis.—The course of the disease is usually slow, 
but recovery should occur if the continuity of the nerve- 
fibre be preserved. Mild cases of traumatic neuritis may 
pass away within a few days. 

Treatment.—If the nerve be cut, the divided ends should 
be sutured on well-known surgical principles. The injured 
part should be placed at rest in a padded splint, or hot 
applications may first be applied for the pain. Electricity 
and massage are of service to the paralyzed muscles. 

Multiple Neuritis. 

Etiology.—The causes of multiple neuritis may be thus 
tabulated: (1) The toxin es of infectious diseases , as diph¬ 
theria, typhoid fever, small-pox, leprosy, scarlet fever, 
syphilis, tubercle, grippe, malaria, and beri-beri; (2) chem¬ 
ical poisons —ether, alcohol, coal-gas, bisulphide of carbon, 
naphtha, lead, arsenic, mercury, phosphorus, copper, zinc, 
ergot, and morphine; (3) auto-toxines with rheumatism, 
gout, arthritis, diabetes, the puerperal state, and chorea; 
(4) cachectic conditions, such as anaemic, cancerous, or tuber¬ 
culous cachexia; (5) idiopathic (?) cases following exposure 
to cold or over-exertion. 

Pathology.—The lesions may be of an interstitial neuritis 
alone, of a parenchymatous neuritis alone, or the two forms 
may be combined. The peripheral parts of the nerves are 
more seriously affected than are the central parts. The 
neuritis may involve motor nerves alone (as in lead¬ 
poisoning), or sensory nerves alone (as in coal-gas poison¬ 
ing) or both sensory and motor nerves may be affected 
(as in alcoholic neuritis). 

Symptoms.—The symptoms are those of neuritis, pre¬ 
viously described, differing only from those of the localized 
form in being more general in their distribution. As the 
symptomatology of multiple neuritis is so varied, it will be 


NEURITIS . 851 

more convenient to describe separately the principal clinical 
types. 

Acute Febrile Polyneuritis .—The onset is acute, with a 
chill, fever of from 103° to 104° F., and pains in the back 
and the limbs. Pain and tingling occur in the peripheral 
parts, and the nerve-trunks are exquisitely tender on pressure. 
Motor weakness becomes evident in a few days, the exten¬ 
sors being the more seriously involved. The paralysis 
rapidly extends up the extremities, and may even involve 
the trunk or the face. The muscles rapidly waste, faradic 
irritability is lost, and the reaction of degeneration appears. 
Trophic changes are commonly observed. The clinical 
picture is that of an acute ascending palsy, resembling or, 
according to some, being identical with Landry’s paralysis. 
Death occurs in from one to three weeks in the severe 
cases. In milder cases, after the symptoms have persisted 
for from four to six weeks slow improvement begins, but 
recovery rarely is complete under one or two years. In 
some cases the onset is more gradual and the course of the 
disease more prolonged, so that the clinical type resembles 
that of Duchenne’s paralysis. 

Alcoholic neuritis , the most common form of the disease, 
occurs more frequently in women than in men. The onset 
may be acute, accompanied by a chill and by fever of from 
ioi° to 103° F.; or the disease may begin gradually, with 
sensory symptoms in the feet and the hands, such as neural¬ 
gic pains, tingling and pricking feelings, and cramps in the 
muscles. There is considerable tenderness along the course 
of the nerve-trunks. Paralysis next occurs, at first in the 
feet, then in the hands and forearms, and the characteristic 
wrist-drop and foot-drop are developed (Fig. 67). The 
affected muscles undergo rapid atrophy and show the reac¬ 
tion of degeneration. The superficial and deep reflexes are 
lost. Sensory symptoms may consist of numbness or ting- 


852 MANUAL OF THE PRACTICE OF MEDICINE. 

ling, or there may be severe neuralgic pains. There may 
be areas of anaesthesia and of retarded sensation. The 
combination of anaesthesia of the skin with extreme hyper- 
aesthesia and soreness of the muscles is highly suggestive 
of the alcoholic form of neuritis. The paralysis may 
remain localized in the hands and feet, and after a stationary 



period of several months slow spontaneous recovery will 
ensue, the duration of the disease being from six to twelve 
months. As the extensors of the feet usually remain para¬ 
lyzed for some time, the “ steppage gait ” becomes promi¬ 
nent and is characteristic of peripheral neuritis. In other 
and more malignant cases there may be spreading paralysis 
of the extremities, trunk, sphincters, and even of the face, 
and death may be caused by involvement of the muscles of 
respiration. 

The cerebral symptoms of alcoholic neuritis are fre¬ 
quently well marked. There may be convulsions at the 
onset or throughout the disease. Delirium with extrava¬ 
gant hallucinations is usually well marked, and may verge 
into the type of delirium tremens. Appreciation of time 
and place is usually lost. In some cases the patient passes 
into the typhoid condition, with low, continued fever and 
muttering delirium. 

Post-febrile Neuritis .—The various forms of post-febrile 









NEURITIS. 


853 


neuritis have been described under the respective diseases 
that precede them. Diphtheritic paralysis, the most com¬ 
mon and serious form, may involve the muscles of the 
palate, eye, or heart, or may be generally distributed in the 
extremities. There are no sensory symptoms in the major¬ 
ity of cases of neuritis following other infectious diseases, 
and the distribution of the paralysis is usually paraplegic. 

Lead-paralysis is usually preceded by anaemia, colic, con¬ 
stipation, and the blue-black line on the margin of the 
gums. The symptoms of lead-palsy may appear abruptly 
or gradually, and are not attended by sensory disturbances. 
The following localized lead-palsies are described : 

1. Anti-brachial type—paralysis of the extensors of the 
fingers and the wrists. The musculo-spiral nerve is in¬ 
volved, causing the characteristic wrist-drop. 

2. Brachial type, involving the deltoid, biceps, brachialis 
anticus, and the supinator longus, more rarely the pectorals. 
This form is bilateral, and may follow the first type or be 
primary. 

3. Aran-Duchenne type, involving the small muscles of 
the hands, closely resembling the earlier stages of progres¬ 
sive muscular atrophy. 

4. Peroneal type, involving the lateral peroneal muscles 
and the extensors of the toes, producing the “ steppage 
gait.” 

5. Laryngeal type, involving the adductors of the larynx. 

In other cases the paralysis becomes more generalized, 

gradually involving the extremities. There are occasionally 
seen acute cases resembling Landry’s paralysis. There has 
been described a rare form of lead-neuritis in which atrophy 
and paralysis come on together and develop proportionately. 

The prognosis of lead-palsy is generally good. The 
course of mild cases is about four months. 

Arsenical paralysis is rare. The symptoms are chiefly 


854 MANUAL OF THE PRACTICE OF MEDICINE . 

motor, resembling those of alcoholic neuritis. The “ step- 
page gait ” is usually well marked. Recovery usually 
occurs in from two to six months. 

Coal-gas neuritis is generally slight, and involves only 
sensory nerves. Numbness persists for a long time in the 
hands and feet. 

Beri-beri, or Kak-ke. —This disease, which occurs 
endemically in Northern Brazil, China, Japan, India, the 
Straits Settlements, and in the Malay Archipelago, is a mul¬ 
tiple neuritis probably due to infection by a micrococcus. 
Foreigners in the endemic localities are usually exempt. 
At times the disease assumes epidemic proportions ; in 1878, 
38 per cent, of the Japanese army were affected. Nothing 
is accurately known as to the etiology. 

Symptoms.—Two principal forms are described—an 
cedematous or “ wet ” and a paralytic or “ dry ” form. The 
oedematous form begins acutely, with fever, oedema, paresis, 
and numbness of the lower extremities. Effusion into serous 
cavities may occur. The liver and spleen are enlarged. 
The dry form may occur primarily or may be a develop¬ 
ment of the wet variety. Sensory symptoms, which are 
prominent, consist of anaesthesia and prickling and tingling 
sensations. Paresis, atrophy, and the “ steppage gait ” 
develop. A malignant form of the dry variety occasionally 
occurs, characterized by rapidly ascending paralysis and by 
suppression of urine. 

The prognosis of the mild forms is good, but relapses are 
common. In some epidemics, however, the mortality is 
over 40 per cent. 

Treatment of Multiple Neuritis. 

Rest in bed is essential, and salicylic acid or the salicy¬ 
lates are recommended during the earlier stages of acute 
cases with fever. Warm applications to the affected limbs 


NEUROMATA. 


855 


should be- made by packs or baths. After the acute stage 
has passed, gentle rubbing of the muscles with oil and mas¬ 
sage are to be employed. Warm baths of 98° F. are to be 
given for half an hour several times a day. Contractures 
are to be overcome by passive movements and by extension. 
The interrupted galvanic current should be employed daily. 
Alcohol should be cut off from all cases, although in the 
alcoholic form the reduction should be gradual. Of drugs 
during the chronic stage, arsenic and strychnine are the 
most valuable. The strength should be supported by care¬ 
ful regulation of the diet, and the use of cod-liver oil is gen¬ 
erally advisable. 


NEUROMATA. 

Tumors situated in the nerve-trunks may be composed 
of nerve-tissue (the true neuromata) or of other tissues (the 
false neuromata). 

False neuromata are chiefly formed of fibrous tissue. More 
rarely there occurs myxomatous tissue, sarcoma, or an in¬ 
filtration of the nerve-fibres by carcinoma. In leprosy the 
nerves are frequently much thickened by an infiltrating 
growth of connective tissue. A curious variety is the plexi- 
form neuroma , which consists of interlacing cords more or 
less nodular. In this condition, which is usually of con¬ 
genital origin, hundreds of fibrous nodules may occur along 
the course of the nerve-trunks. The symptoms of false 
neuromata are seldom evident, although in some cases the 
symptoms of neuritis may appear. 

True neuromata , containing nerve-fibres, rarely ganglionic 
cells, may form small subcutaneous painful tumors 
tubercula dolorosa. These tumors are not always, now- 
ever, pure neuromata, but may consist of fibrous tissue 
or may be adenomatous growths of the sweat-glands. 
True neuromata may develop on the cut ends of nerves 


856 MANUAL OF THE PRACTICE OF MEDICINE. 


in amputation-stumps, in which situation they may lead 
to great pain and distress. 

Treatment.—When painful, the growths may be excised. 

NEURALGIA. 

Etiology.—Under the term “ neuralgia ” are included 
painful affections of the nerves due either to functional dis¬ 
turbance or to neuritis. The causes and symptoms of neur¬ 
itis have elsewhere been described. 

Members of neurotic families are subject to neuralgic 
affections. Women are more often affected than are men, 
but children are usually exempt. 

General debility, anaemia, excesses, over-work, and ner¬ 
vous exhaustion are potent predisposing factors. Neuralgia 
is not uncommon with malaria, rheumatism, gout, syphilis, 
diabetes, and chronic lead-poisoning. Reflex irritation may 
act as an exciting cause; thus obstinate trifacial neuralgia 
may result from carious teeth or from eye-strain. In sus¬ 
ceptible patients exposure to wet and cold may induce an 
attack. 

Pathology.—Aside from the cases in which neuralgia is 
dependent upon neuritis, the disease is a pure neurosis. 

Symptoms.—The attack may be preceded by chilliness, 
mental depression, or tingling in the part to be affected. 
The chief symptom is pain, of a paroxysmal, stabbing, burn¬ 
ing, or darting character, localized in certain groups of 
nerves. The skin of the affected area may be hyperaesthetic, 
and spots of exquisite tenderness are detected at certain 
points along the nerve where it makes its exit through a 
bony canal or a fibrous sheath. Vaso-motor symptoms may 
accompany the pain; the skin may be cool, or hot and 
burning, and there may be areas of oedema or of erythema 
or herpes. Twitching of the muscles, or even spasms, may 
occur during the paroxysm. The attack lasts from a few 


NEURALGIA. 


857 


minutes to a number of hours and then subsides. The 
interval between the paroxysms varies in different cases. 
Frequently the recurrences are at regular intervals, often 
only at the menstrual period. 

Clinical Varieties.— Trifacial Neuralgia (Tic Douloureux). 
—The pain is felt in one or more branches of the nerve, the 
ophthalmic division being most frequently affected. Hyper- 
sesthesia of the skin and of the mucous membranes is com¬ 
mon, and vaso-motor phenomena are not infrequently pres¬ 
ent—flushing, sweating, salivation, increased nasal discharge, 
and lachrymation. There may be trophic changes—ery¬ 
thema, induration of the skin, loss of hair or local grayness. 
In severe cases there may be an associated spasm of the 
facial muscles—the “ tic convulsif.” Tender points corre¬ 
spond to the supraorbital, infraorbital, and mental foramina, 
less frequently to the occipital protuberance and the upper 
cervical spine. Trifacial neuralgia is frequently of reflex 
origin. 

Ccrvico-occipitalNeuralgia. —The pain, which is usually dull 
and more or less constant, is localized over the back of the 
neck and the head, extending forward as far as the parietal 
eminences and the ear. There is frequently hyperaesthesia of 
the scalp. The most important tender point is located mid¬ 
way between the mastoid process and the spine, where the 
great occipital nerve becomes superficial. Exposure to cold 
and cervical caries are the most frequent causes of this 
form of neuralgia. 

Cervico-brachial neuralgia , which involves the sensory 
nerves of the brachial plexus, is usually most intense in the 
axilla or along the course of the ulnar nerve. When the 
circumflex nerve is involved the pain is in the deltoid. The 
pain may be so increased by movement as to render the 
arm helpless. The most common tender points are the 
axillary, the circumflex at the posterior border of die del- 


858 MANUAL OF THE PRACTICE OF MEDICINE . 

toid, the superior ulnar behind the elbow, and the inferior 
ulnar in front of the wrist. Cervico-brachial neuralgia more 
frequently than any other form is the result of injury. Some 
severe forms are evidences of an occupation-neurosis. 

Intercostal neuralgia is very common in hysterical and 
anaemic women. Pain is felt along the intercostal nerves in 
aneurysm, caries, and pleurisy. There is usually a dull, 
constant pain, with acute stabbing exacerbations. Painful 
points are detected beside the vertebra, under the angle of 
the scapula, and under the breast. Pleurodynia differs 
from true intercostal neuralgia in being localized in one 
spot not corresponding with the course or exit of the inter¬ 
costal nerves. The pain is increased by expansion of the 
thorax rather than by lateral movements of the trunk. 
Herpes zoster occurs with the most aggravated form of 
intercostal neuralgia, which may persist after the eruption 
has subsided. The eruption and the neuralgia are due to 
neuritis. 

Lumbar neuralgia gives rise to pain along the crest of the 
ilium, the inguinal canal, and the spermatic cord, and in the 
testis, scrotum, and labium majus. Irritable testis is usually 
accompanied by syncopal sensations. 

Coccygodynia , which is common in women, is aggravated 
by the sitting posture. This form of neuralgia is usually 
very intractable. 

Sciatica .—The pain extends down the back of the thigh, 
often reaching as far as the foot. The pain may be uni¬ 
formly distributed along the course of the nerve, but not 
infrequently there are spots in which it is more intense. 
The pain is usually more or less constant and of a gnawing, 
burning character, but it may be paroxysmal, the paroxysms 
being usually more intense in damp weather and at night. 
The pain is regularly increased by walking; the knee is 
bent and the patient walks on the toes to diminish the ten- 


NEURALGIA. 


859 


sion on the nerve. The painful points are located (1) above 
the hip-joint, near the posterior iliac spine, (2 ) at the sciatic 
notch, (3) about the middle of the thigh, (4) behind the knee, 
(5) below the head of the fibula, (6) behind the external 
malleolus, and (7) on the back of the foot. Tenderness is 
usually also elicited by pressure along the course of the 
nerve. Muscular wasting and fibrillary twitchings compli¬ 
cate the severe cases. 

Sciatica is most common in those with a gouty or rheu¬ 
matic tendency. The nerve may be compressed by intra- 
pelvic growths or may be involved by spinal caries. 

The prognosis must be made with caution, as many cases 
of neuralgia prove intractable to treatment. 

Treatment.—All causes for reflex irritation must be dis¬ 
covered and removed if possible. A tonic and supporting 
treatment is of the greatest importance. The patient should 
be built up in every possible way. Iron and arsenic are 
required for anaemic conditions; gouty and rheumatic taints 
are to be treated; quinine is to be given to malarial patients. 
The diet should be generous. Fats are indicated in nearly 
all of the cases, and a liberal amount of meat is to be allowed 
to all except those subject to gout. Many obstinate cases 
are benefited by residence in a dry inland climate. Strychnine, 
phosphorus, and cod-liver oil are of great service. 

For the pain, antipyrine, phenacetine, lactophenin, chloral, 
croton-chloral, the bromides, and cannabis indica may be 
given. Aconite and gelsemium are recommended for tri¬ 
facial neuralgia. Morphine, codeia, and hypodermic injec¬ 
tions of cocaine are to be withheld, because of the danger 
of forming the habit. Local applications are frequently of 
service. Heat, stimulating liniments, fieezing of the skin 
by ether or methyl-chloride sprays, blisters, or application 
of the actual cautery may be employed. Surgical treatment 
may be required for obstinate cases. Nerve-stretching is 


86o MANUAL OF THE PRACTICE OF MEDICINE. 


not likely to be followed by permanent results. Neurectomy, 
or the excision of a portion of the affected nerve, is fre¬ 
quently followed by good results, but the pain may return 
in time. 


7. GENERAL NERVOUS DISEASES. 

INFANTILE CONVULSIONS; INFANTILE 

ECLAMPSIA. 

Etiology. —Convulsions are so frequent in children that a 
special mention is justifiable. Owing to the lack of develop¬ 
ment of the higher cerebral centres of children, the lower 
centres are but improperly controlled, so that increased 
reaction to direct or reflex stimulation is permitted. The 
most important causes for convulsive seizures in children 
are the following: 

1. Rickets. —Convulsions, usually without marked febrile 
disturbance, occur from slight causes, and are apt to be 
repeated at intervals for months. 

2. Gastro-intestinal Irritation. —This most common cause 
arises from dietetic errors, indigestion, or worms. The 
convulsions are usually accompanied by fever. 

3. General exhaustion , especially if due to diarrhceal 
disease. Convulsions may be part of a hydro-encephaloid 
condition. 

4. Mechanical congestion of the brain, as with violent 
attacks of coughing. 

5. Deficient aeration of blood , as with croup, diphtheria, 
or vitiated air in incubators. 

6. During the first few days of life, from severe brain- 
injury during birth. If the convulsions be severe and per¬ 
sistent, meningeal hemorrhage should be suspected. 

7. Peripheral irritation , as teething, phimosis, or otitis. 



INFANTILE CONVULSIONS . 861 

8. Acute febrile conditions, especially at the onset of 
measles, scarlet fever, and pneumonia. 

9. Convulsions may usher in or accompany any serious 
disease of the nervous system in children. 

10. Convulsions in infancy are not infrequently epileptic. 

The symptoms may be preceded by signs of irritation 

of the nervous system—restlessness, irritability, and twitch- 
ings. The attack begins with a fixation of the eyeballs; 
the face becomes pale, the limbs and trunk become rigid 
and stiff. The fingers and toes are inverted (carpopedal 
spasm). Respiratory movement is impaired, so that the 
face becomes cyanotic. The spasm may relax, or may 
become clonic as in epilepsy. In some cases clonic spasms 
are marked from the start, and usually begin in the hands 
and face. 

The spasm may be followed by muscular rigidity for 
some little time. In convulsions due to indigestion the 
attack may be single; in other cases attacks follow each 
other with great rapidity. Attacks coming irregularly and 
without assignable cause in children over two years of age 
are likely to prove to be true epilepsy. Convulsions may 
be followed by slight paresis or may lead to meningeal 
hemorrhage with hemiplegia. 

The prognosis is usually good. A dubious prognosis 
should be given, however, in the case of weakly subjects, as 
fatal exhaustion may be induced. 

Treatment. —The first and most important measure is to 
search for the cause of the seizure, and to remove it if 
possible. If indigestion be the cause, a prompt emetic 
should at once be given, or the stomach may be washed 
out. For the attack itself, if severe, whiffs of chloroform 
should be given, and an enema containing chloral (gr. ij) 
and sodium bromide (gr. v-x) should be administered, these 
doses being suitable for a child of from six to twelve 


862 MANUAL OF THE PRACTICE OF MEDICINE. 


months. No time should be lost in immersing the child in 
a bath at 95 0 F.; baths of a higher temperature are not 
suitable. After the bath an ice-cap should be employed or 
cold applications should be made to the head. Morphine 
may be necessary in case of recurring convulsions, but the 
drug should be administered with extreme caution, and 
should never be ordered for infants under six months of 
age. For a child of one year, gr. to hypodermically 
will be a sufficient dose. 

EPILEPSY. 

Etiology. —Among the remote causes which induce this 
disease, heredity is the most important, a neurotic family 
history being obtained in about one-quarter of all cases. 
A direct inheritance of epilepsy is rare, but the parents are 
apt to suffer from nervous diseases or to be the victims 
of the alcohol habit. Any vicious influence deteriorating 
the parent stock predisposes to the development of epi¬ 
lepsy in the offspring. Consanguineous marriages exert 
a distinct influence upon the causation of the disease. 
Epilepsy may interchange with insanity in different gen¬ 
erations. 

An immediate exciting cause is determined in but one- 
third of all cases. There may be blows on the head, dissi¬ 
pation, fright, or continued reflex irritation. Many cases in 
children date from teething or from acute infectious diseases. 
Although in many cases the exciting cause may be removed, 
the nerve-centres may have formed the habit of discharging 
nerve-force, so that the seizures continue through life. 

Males are more frequently affected than females. The 
disease appears before the thirteenth year in one-third of 
the cases, between the thirteenth and nineteenth years in 
one-third, and between the nineteenth and thirtieth years in 
one-third of the cases. After the thirtieth year idiopathic 



EPILEPSY. 863 

epilepsy is rare. “An epilepsy which develops after the 
thirty-fifth year of age is not idiopathic, but is due to some 
organic brain disease, to the abuse of alcohol, to reflex irrita¬ 
tion, or other causes, which in some cases may be so hidden 
as to be exceedingly difficult of recognition ” (H. C. Wood). 
In the great majority of cases, recurring epileptic seizures 
in those over the age of thirty are due to brain syphilis. 

The pathology of epilepsy is obscure. A degeneration 
of the neuroglia in the brain has been described by some 
observers. The generally accepted theory is that the seiz¬ 
ures are due to a discharging lesion of the brain-cortex, so 
that an overflow of nerve-force occurs. 

Symptoms.—Loss of consciousness with general convul¬ 
sions is known as grand mal; loss of consciousness with¬ 
out convulsions, as petit mal. Localized convulsions, 
usually without loss of consciousness, are described as 
Jacksonian or cortical epilepsy. 

Grand Mal. —The attack may be preceded by peculiar 
sensations, described as aurce , which give warning to the 
patient that an attack is impending. Sensory aurae are the 
most common; they differ in character in different patients, 
but are constant in the one subject An aura consists of a 
peculiar sensation, felt in some part of the body, mounting 
upward to the head. Aurae of special senses are occasion¬ 
ally observed. An ocular aura consists of visual sensa¬ 
tions—flashes of light or of color, bizarre forms, double 
vision, or even blindness. In auditory aurae abnormal 
sounds or voices may be heard. An olfactory aura, which 
takes the form of a bad smell, is rather infrequent. Psy¬ 
chical aurae are not uncommon; the patient may feel 
alarmed or may be in terror, or there may be a vague sense 
of strangeness or a dreamy sensation. In some cases the 
attack is preceded by forced movements ; the patient may 
run forward with great speed (“ procursive epilepsy ”), or 


864 MANUAL OF THE PRACTICE OF MEDICINE. 

may turn rapidly around as if on a pivot. In many cases 
the aura is absent. 

The fit is usually abrupt; the patient falls to the ground 
unconscious. Preceding the attack there is generally a 
wild, harsh scream or groan. The fit occurs in three 

stages: 

1. Tonic Spasm .—The head, eyes, and mouth are rotated 
to the side on which the spasm is more intense; the body 
is stiff and rigid. The hands are clenched, the arms and 
forearms flexed, the legs extended, and the feet extended 
and inverted. The body, however, is not always distorted 
in the same manner, as the muscular spasms may not be 
equally intense. The face, at first pale, becomes dusky or 
livid, owing to the respiratory spasm. The tonic stage lasts 
for from a few seconds to one or two minutes. 

2. Clonic Stage .—Tremulous vibrations occur in the mus¬ 
cles ; the vibrations increase in range until the limbs are 
jerked and tossed violently about. The face is frightfully 
contorted, foamy saliva is forced from the mouth, and the 
tongue is apt to be severely bitten. Respirations are noisy 
and stertorous. Urine and feces may be passed involun¬ 
tarily, especially in nocturnal attacks. The pupils are im¬ 
movably dilated, and after the attack usually show remark¬ 
able oscillations. The temperature is usually normal, but 
in case the attack be prolonged a slight rise, rarely to 102° 
F., may be observed. The clonic stage lasts for three or 
four minutes, and the patient passes into the— 

3. Stage of Coma .—The patient becomes quiet and passes 
into a deep sleep, awakening after a few minutes or hours 
with headache, mental confusion, and muscular soreness. 
After the attack the reflexes are usually increased. The 
urine is usually increased in quantity after the attack, and 
may contain albumin. In rare instances the patient passes 
from one spasm into another without regaining conscious- 


EPILEPSY. 865 

ness. In this status epilcpticus the temperature may rise to 
107° F., and the patient is apt to die from exhaustion. 

Post-epileptic Symptoms. —The patient may emerge from 
the coma in a peculiar trance-like condition, and may per¬ 
form purposeless and incongruous actions, at times so appar¬ 
ently rational that it may be impossible to believe that the 
patient is not conscious. At times this condition of epileptic 
automatism passes into the condition of epileptic mania, in 
which condition the patient is dangerous or even homicidal. 
After the attack slight transient hemiplegia or aphasia 
may be noticed. Epilepsy is frequently succeeded by 
mental degradation which may ultimately lead to complete 
dementia. 

Nocturnal epilepsy may occur without the patient’s know¬ 
ledge, so that the condition may exist for years before the 
diagnosis is suspected. 

2. Petit Mal. —The ordinary type consists of sudden 
loss of consciousness. The patient suddenly stops what he 
is doing, the face becomes pale and fixed, the pupils dilate; 
but after a few seconds consciousness is regained and the 
patient resumes his work or conversation as if nothing had 
happened. Aurae are infrequent in petit mal. In some 
instances the attack consists of forced movements, such as 
the sudden running forward of procursive epilepsy. In 
other cases, during the attack the patient may perform 
some automatic action, such as undressing himself or tear¬ 
ing to pieces whatever may be within reach. There may 
be sudden outbursts of maniacal excitement during which 
crimes and assaults may be committed: these cases of 
“ masked epilepsy ” are of great medico-legal interest. 
Somnambulistic epilepsy consists in the performance of 
accustomed acts while in a somnambulistic state. 

Attacks of petit mal terminate in some instances in facial 
twitchings or in hysteroid convulsive movements. The 
55 


866 MANUAL OF THE PRACTICE OF MEDICINE. 


various manifestations of petit mal are exceedingly varied. 
In the majority of cases attacks of grand mal ultimately 
develop, and the two forms may alternate. 

3. Jacksonian epilepsy, which is regularly due to irrita¬ 
tive lesions of the motor centres, especially of the motor 
cortical zone, differs from true epilepsy in the fact that con¬ 
sciousness is retained. 

The spasm occurs in limited groups of muscles, which 
are always the same in each patient. Preceding the attack 
there may be numbness or tingling of the affected part. 
In growing lesions the march of the spasm may be observed, 
and accurate localization becomes possible. 

Diagnosis. —Petit mal may be mistaken for syncope, 
vertigo, or indigestion, but in these conditions conscious¬ 
ness is not lost. Jacksonian epilepsy is rarely mistaken 
for other conditions. Localized spasms may, however, 
occur in uraemia and in progressive paresis. 

Grand mal is to be diagnosed from uraemia, simple 
convulsions in children, convulsions from organic brain 
disease, malingering, and hystero-epilepsy. Uraemia is 
diagnosed by the high arterial tension, the scanty and 
albuminous urine, and the presence of fever during the 
attack. 

Simple convulsions in children are usually due to some 
recognized cause and are not apt to be repeated. Convul¬ 
sions due to organic brain disease, such as tumors of the 
cerebellum and progressive paresis, are to be diagnosed by 
attention to the history and the other symptoms. Malin¬ 
gerers may closely simulate epilepsy, but the tongue is not 
bitten, foaming at the mouth does not occur, and strong 
pressure by the thumbs over the supraorbital notches will 
rapidly cut short the attack. The diagnosis from hystero- 
epilepsy is to be made by the following points, thus tabu¬ 
lated by Gowers : 


EPILEPSY. 


867 



Epileptic. 

Hysteroid. 

Apparent cause . , 

None. 

Emotion. 

Warning .... 

Any, but especially unilat- 

Palpitation, malaise, chok¬ 
ing. bilateral foot-aura. 

Onset . 

eral or epigastric aune. 

Always sudden. 

Often gradual. 

Scream. 

At onset. 

During course. 

Rigidity or “struggling,” 

Convulsion . . . 

Rigidity followed by “jerk- 

Biting . 

mg,” rarely rigidity alone. 

throwing about of limbs 
or head, arching of back. 

Tongue. 

Lips, hands, or other people 
or things. 

Micturition . . . 

Frequent. 

Never. 

Defecation . . 

Occasional. 

Never. 

Talking. 

Never. 

Frequent. 

Duration .... 

A few minutes. 

More than ten minutes, often 
much longer. 

Restraint necessary 

To prevent accident. 

To control violence. 

Termination . . . 

Spontaneous. 

Spontaneous or induced 
(water, etc.). 


The prognosis for cure, except in Jacksonian epilepsy, is 
bad, but the disease may be materially relieved by treatment. 
The prognosis is better in cases coming on in adults, due 
to syphilis, and in children in cases where the convulsions 
have followed teething or acute fevers. Epilepsy does not 
tend materially to shorten life. 

The question of the intellectual future of the patient is 
always a serious one. Mental degradation occurs in a con¬ 
siderable proportion of cases, but epilepsy is not necessarily 
incompatible with an active and useful life. 

Treatment.—In cases of reflex or of Jacksonian epilepsy 
the cause of the irritation should be removed. In some 
cases the results are brilliant, but in many instances there is 
but partial improvement, the habit of nerve-discharge of 
the higher centres having been established. In cases of 
epilepsy in which the aura is slow, attempts should be made 
to check the spasm by the inhalation of amyl nitrite; or in 
case of ascending sensory aura of an extremity, the patient 
should be taught to encircle the part firmly with the hand 
or with a tight bandage. Unfortunately, the aurae are 













868 MANUAL OF THE PRACTICE OF MEDICINE. 


usually of too short duration to allow of any preventive 
treatment. 

During the attack the patient should be placed in a 
horizontal position, the clothing loosened, and a gag firmly 
placed between the teeth, to prevent the tongue from being 
bitten. Inhalations .of chloroform or of ether are per¬ 
missible in protracted or severe paroxysms, or a hypodermic 
injection of morphine may be administered. 

Dietetic and Hygienic Treatment .—The patient should do 
all things in moderation, never in excess. Marriage should 
be interdicted. Habits of firm but kindly discipline are im¬ 
portant for growing epileptic children. The diet should be 
chiefly, but not altogether, vegetable; meat, however, may be 
allowed once a day. The patient should be restrained from 
going to bed until gastric digestion has been completed. 

Medicinal Treatment .—Bromides are the most serviceable 
drugs in the treatment of epilepsy. Of the various bromides, 
the salt of sodium is the most preferable. The bromide 
treatment should be pushed until mild affects of bromism— 
acne, mental depression, foul breath, and muscular weakness 
—have been produced, and should then be reduced so that 
the patient is kept just within the physiological action of 
the drug, so that the palate-reflex is lost. As a rule, from 
y 2 to i y 2 drams daily are sufficient for an adult. The drug 
should be largely diluted in water or in milk, and the liabil¬ 
ity to acne is said to be diminished by the joint administra¬ 
tion of arsenic. The bromide treatment should be continued 
for at least two or three years after the cessation of the 
attacks. 

The combination of antipyrine with the bromides is fre¬ 
quently of service. Wood claims that a mixture of bromide 
of ammonium (gr. xx-xxx), antipyrine (gr. vij), and Fowler’s 
solution (Tft ij-iij) affords the best combination known for 
the majority of cases, the indicated doses being admin- 


PARALYSIS AG/TANS. 869 

istered twice daily. Sulphonal may also be given advan¬ 
tageously with the bromide treatment. 

Among other forms of treatment employed for their 
alleged specific action are valerian, belladonna, oxide of 
zinc, and nitrate of silver and borax, but these drugs prove 
almost worthless when tried. 

PARALYSIS AGITANS. 

Etiology and Synonyms. —Paralysis agitans usually ap¬ 
pears between the fiftieth and sixtieth years, and is rare be¬ 
fore the age of forty. Men are more commonly attacked than 
women, in the proportion of 5 : 3. Hereditary influences can 
be traced in 15 per cent, of all cases. In about one-third of all 
cases an exciting cause can be ascertained—emotion, fright, 
exposure to cold, physical fatigue, or acute disease. In other 
cases the disease begins without known cause. It is not 
a disease of vice. Synonyms: Shaking palsy; Parkinson’s 
disease. 

Pathology. —No lesions are found to account for the con¬ 
dition, but it is supposed that the symptoms are due to pre¬ 
mature senile changes in the cerebral cortex. 

Symptoms. —The characteristic symptoms are tremor and 
muscular rigidity. 

The tremor develops insidiously, and usually appears first 
in the hands or the fingers. At first the tremor may be 
controlled by the will, but later it becomes more continuous 
and cannot be controlled. The tremors are short, rapid 
(being about 5 to the second), and in the fingers may be 
rhythmical, so that the motion resembles that produced by 
rolling some small body between the thumb and the fingers. 
The handwriting shows the character of the fine tremors. 
It is peculiar for the tremor to continue when the hand or 
the limb is at rest and to cease during voluntary motions, 
so that the patient may safely carry a glass of water to the 



870 MANUAL OF THE PRACTICE OF MEDICINE. 

lips. In other cases the tremor cannot be thus checked, 
and in rare instances it may even be increased by voluntary 
motions. Emotions regularly increase the tremor. The 
tremor extends to various parts of the body without fixed 
order of progression, but the face is rarely involved. Vol¬ 
untary motions are performed slowly and with but little 
power. 

Muscular rigidity , which is characteristic of the advanced 
stages of the disease, gives rise to changes in the attitude, 
the gait, and the facial expression. The attitude is charac¬ 
teristic (Fig. 68); the body is inclined forward, and the ex¬ 
tremities are in a general 
condition of flexion. The 
inclination of the body 
forward may throw the 
patient in front of the cen¬ 
tre of gravity, so that he 
will have to walk faster 
and faster, or even to 
run, to avoid falling for¬ 
ward—the so-called “ fes- 
tinating gait.” The face 
is fixed, expressionless, 
and immobile; the eye¬ 
brows are raised, giving 
a characteristic facies to 
which the name “ Park¬ 
inson’s mask ” has been 
applied. The voice is a high-pitched monotone. 

Sensory symptoms consist of soreness and a sense of 
fatigue in the affected muscles. Various vaso-motor symp¬ 
toms may occur. The surface-temperature over the affected 
muscles may be increased. Mental derangement does not 
occur, although the patients may become emotional. The 




Fig. 68.—Paralysis agitans (St. Leger). 







ACUTE DELIRIUM. 87 1 

urine may contain an excess of phosphates, or there may 
be polyuria. 

Diagnosis. —Disseminated sclerosis develops earlier in 
life, nystagmus is present, the speech is scanning, and there 
is no characteristic attitude. The diagnosis from post¬ 
hemiplegic tremor is readily made by the history of the 
case, the increased reflexes, and the hemiplegic distribution 
of the latter disease. Senile tremor is rare under the age 
of seventy, and is usually marked in the muscles of the 
neck, producing slight movements of the head. Toxic 
tremors from alcohol or from tobacco usually occur only 
on motion, and the tremor is more pronounced, showing 
considerable range. 

Prognosis. —The condition is incurable, but it does not 
tend to shorten life. 

Treatment. —A number of drugs have been recom¬ 
mended, but no form of treatment seems to have any per¬ 
manent influence upon the disease. Mental and physical 
rest should be enjoined, and prolonged lukewarm baths 
may be advised. Hyoscine hydrobromate (gr. yjy-Q gradually 
increased) has been given with temporary benefit. Dana 
has used the bromide of uranium (gr. -^) with apparently 
good results. Arsenic may also be used. 

ACUTE DELIRIUM. 

Etiology and Synonyms. —Acute delirium usually occurs 
during active adult life, and may be due to alcoholism, to 
profound grief, or to over-work; or the condition may 
appear as a sequel to sunstroke, fevers, or injuiies to the 
head. Synonyms .* Bell s mania ; Acute penencephahtis. 

Pathology— The nature of the disease is unknown. By 
some authors the lesion consists of hyperaemia and oedema 
of the brain and its membranes, with a choking of the 
lymph-channels of the pia and of the cortex by leucocytes. 


Sy 2 MANUAL OF THE PRACTICE OF MEDICINE. 

According to others, the symptoms are due to nerve¬ 
poisoning by unknown toxic products. 

Symptoms.—The onset may be preceded by the prodro¬ 
mal symptoms of irritability, restlessness, and insomnia. 
The developed disease presents two stages, one of maniacal 
delirium, the other of apathy, collapse, and coma. The 
delirium comes on rapidly and reaches a grade of wild 
frenzy with hallucinations and delusions. There is absolute 
insomnia. The temperature ranges between 102° and 105° 
F., but falls to subnormal in the advanced stages. The 
stage of mania lasts for from a few hours to several days 
and is succeeded by a stage of quiet in which the patient 
lies semi-comatose, responding incoherently when aroused. 
In the advanced stage the pulse fails and the symptoms of 
collapse become evident. There may be irregular desqua¬ 
mation of the skin, ulceration, gangrene, pemphigus, or areas 
of complete anaesthesia. 

The diagnosis should be made from the following con¬ 
ditions : (1) Masked pneumonia with maniacal delirium at the 
onset; (2) acute uraemia with mania followed by coma; 
( 3 ) typhoid fever with marked cerebral symptoms at the 
onset; (4) delirium tremens; (5) acute meningitis. 

Prognosis.—The duration of the disease is about a week, 
but it may be protracted for two or three weeks. The 
disease is almost uniformly fatal. When recovery occurs 
the mind is almost regularly affected. 

Treatment.—During the maniacal stage the patient should 
be actively purged, and in robust cases free venesection 
should be resorted to. The patient is to be quieted by 
morphine, hyoscine, or chloral, and when tractable the cold 
bath or cold pack may be employed for its calmative effect. 
Good results are claimed for the hypodermic use of ergotine 
in large doses, 15 grains being given every eight hours. 


CHOREA. 


S/3 


CHOREA. 

Etiology and Synonyms.—The disease is more common 
in females than in males, and three-fourths of all cases 
occur between the ages of five and fifteen. Chorea is rare 
before the fourth year. Negroes are usually exempt. The 
disease is most common in high-strung, nervous, excitable 
children, especially those who are ambitious at school. 
The exciting cause in 15 per cent, of all cases is fright, 
but mental worry, grief, or sudden trouble may also pre¬ 
cipitate an attack. Ocular defects and reflex irritation do 
not seem to produce true chorea. An antecedent history of 
rheumatism is obtained in about one-fifth of the cases. In 
only 2 per cent, of the cases does chorea antedate the rheu¬ 
matic complaint. Chorea may occur after certain infectious 
diseases—scarlet fever, whooping-cough, gonorrhoea, sec¬ 
ondary syphilis, and septic infections—and may also com¬ 
plicate pregnancy, especially in primiparse during the first 
five months. Synonyms: St. Vitus’s dance; Sydenham’s 
chorea. 

Pathology.—There are no characteristic lesions in chorea. 
In some cases vascular changes are found in the nervous 
system—hyaline transformation, exudation of leucocytes, 
small punctate hemorrhages, and thrombosis of the smaller 
arteries—but these changes are inconstant. Endocarditis is 
the most frequent lesion found at autopsies, occurring in 
about 90 per cent, of the cases. The endocarditis may be 
of the malignant variety. 

The nature of the disease-process in chorea is not yet 
accurately known; three theories for its causation are 
advanced: (1) That chorea is a functional brain disorder, 
leading to an instability of the nerve-cells controlling the 
motor apparatus, induced by hypersemia or anaemia, by 
psychical influences, or by central or reflex ii 1 itation. (2) 


8/4 MANUAL OF THE PRACTICE OF MEDICINE. 

That chorea is due to embolism of the smaller cere¬ 
bral arteries. This view is favored by the experimental 
production of chorea in animals by injecting fine insolu¬ 
ble particles into the carotids. All cases of chorea, how¬ 
ever, cannot be thus explained, as histological examination 
of the brain may be negative. (3) That chorea owes its 
origin to a microbic infection at present unknown. This 
view seems highly probable, although it does not explain 
why chorea is so frequently excited by fright or other 
psychical disturbance. 

Symptoms.—The disease may begin abruptly or may 
be preceded by prodromata. The child becomes restless, 
is fidgety, irritable, and emotional. 

Three grades of the developed disease are described by 
Osier: 

1. Mild chorea , in which the muscular affection is slight, 
speech is not seriously affected, and the general health 
remains good. In the mild cases there are constant irregu¬ 
lar, jerky motions involving usually a hand or a hand and 
the face. There may only be awkwardness or slight inco¬ 
ordination of voluntary motions. 

2. The severe form , in which the choreic movements be¬ 
come general, and are so pronounced that the patient cannot 
get about, feed, or undress himself. The speech is usually 
affected, and there may be motor weakness on one side or 
in the limb most affected. 

3. The maniacal form , or chorea ins aniens, characterized 
by profound cerebral disturbances and by violent choreic 
motions. There is active delirium, and there may be hyper¬ 
pyrexia, especially in the fatal cases. 

The individual symptoms may be thus described : 

I. Motor symptoms may not pass beyond awkwardness or 
slight inco-ordination, or they may develop into unwilled 
clonic spasms of various parts. The hands are usually 


CHOREA. 


8 ; 5 


first involved, then the face and subsequently the legs. The 
movements may be confined to one side—hemichorea. The 
attack usually begins on the right side, but in rarer instances 
the movements may be general from the start. The muscles 
of the trunk and of the thighs are usually bilaterally affected. 

In about one-fourth of the cases the speech becomes 
affected, from involvement of the lips and tongue. In mild 
cases there is merely embarrassment or hesitancy; in 
severer cases articulation becomes jumbled and incoherent, 
so that the child ceases from attempts to talk. The in¬ 
spiratory muscles may be affected, so that the patient will 
emit sighing or odd barking sounds. Choreic movements 
generally cease during sleep. There is no evidence that 
the muscles of the gastro-intestinal tract, the bladder, the 
rectum, or the bronchi are ever affected, and irregular con¬ 
tractions of the papillary heart-muscles probably do not 
exist. 

Muscular zveakness is not uncommon, and rarely amounts 
to more than an enfeeblement of the grip or a dragging of 
the foot. In other cases there may be more evident paresis, 
either of the hemiplegic, paraplegic, or monoplegic type 
(“ paralytic chorea ”). 

2. Sensory Disturbances .—Pain in the muscles of the 
affected limbs is uncommon, but pain and tenderness 
along the nerve-trunks may be marked, especially in cases 
of hemichorea. Numbness and tingling or pricking sen¬ 
sations are occasionally encountered. Multiple neuritis may 
occur. Headache is frequent and may be persistent. 

Mental symptoms are rarely absent, although rarely are 
they pronounced. There may be irritability of temper with 
emotional outbreaks, and a change in the moral character 
of the child. Memory and aptitude for study are impaired. 
Melancholia is not uncommon. In rare instances dementia 
develops. Aggravated cases of chorea, the chorea insaniens, 


876 MANUAL OF THE PRACTICE OF MEDICINE. 

are characterized by delusions, hallucinations, delirium, and 
even mania. 

The reflexes in chorea may be normal; in one-half the 
cases the knee-jerk is diminished or lost. Cutaneous affec¬ 
tions are common in chorea, but are generally due to the 
arsenic treatment or to allied rheumatic affections. The 
skin affections embrace erythematous and papular pigmen¬ 
tations, rashes, herpes zoster, erythema nodosum, and pur¬ 
pura rheumatica. Fever occurs in about one-eighth of all 
cases, and is usually slight. Any febrile condition other 
than a slight transient rise of temperature is indicative of 
some complication—rheumatic arthritis, pericarditis, or en¬ 
docarditis. Fatal cases of chorea insaniens are usually 
accompanied by a high ante-mortem temperature. 

Heart Symptoms .—Neurotic palpitation is not uncommon. 
Cardiac murmurs occur in from 25 to 30 per cent, of all 
cases, and may be either of haemic or of organic origin. 
Haemic murmurs are most commonly observed between the 
third and fourth weeks. Acute choreic endocarditis rarely 
gives rise to symptoms. The following statements are 
given by Osier: 

“ In thin, nervous children a systolic murmur of soft 
quality is extremely common at the base, particularly at 
the second left costal cartilage, and is probably of no 
moment. 

“ A systolic murmur of maximum intensity at the apex, 
and heard also along the left sternal margin, is not uncom¬ 
mon in anaemic, enfeebled states, and does not necessarily 
indicate either endocarditis or insufficiency. 

“ A murmur of maximum intensity at apex, with rough 
quality, and transmitted to axilla or angle of scapula, indi¬ 
cates an organic lesion of the mitral valve, and is usually 
associated with signs of enlargement of the heart. 

“ When in doubt it is much safer to trust to the evidence 


CHOREA. 


877 


of eye and hand than to that of the ear. If the apex-beat 
is in the normal position, and the area of dulness is not 
increased vertically or to the right of the sternum, there is 
probably no serious valvular disease. 

“ The endocarditis of chorea is almost invariably of the 
simple or warty form, and in itself is not dangerous; but it 
is apt to lead to those sclerotic changes in the valve which 
produce incompetency. Of 110 choreic patients examined 
more than two years after the attack, 54 presented signs of 
organic heart disease. 

“ Pericarditis is an occasional complication of chorea, 
usually in cases with well-marked rheumatism.” 

The diagnosis is usually evident. Chorea should not 
be mistaken for spastic diplegia in children, for cerebral 
atrophy, or for Friedreich’s ataxia. In the former case the 
onset in infancy, the steady and chronic course, increased 
reflexes and muscular rigidity, and the impaired intellect 
are distinguishing features. In Friedreich’s ataxia the 
scanning speech, spinal curvature, nystagmus, deformities 
of the feet, and the slow, inco-ordinate movements render 
the diagnosis easy. Hysteria may closely resemble chorea, 
but the movements are rhythmic and not choreiform in 
character, and other hysterical symptoms are present. 

Prognosis. —Recovery is the rule, although there exists 
in chorea a tendency to recurrences, especially in rheumatic 
cases. Recurrences are most frequent during the spring 
months. The total mortality is about 2 per cent. The 
mildest cases get well in two or three weeks. The ordinary 
duration is about two months, but cases may drag along 
for from three to six months. The ultimate prognosis, how¬ 
ever, is that of the associated cardiac lesions. 

Treatment. —Excessive brain-work and ev e 
school, and the competing for prizes, should be prohibited 
in nervous children, especially in those who have had pre- 


878 MANUAL OF THE PRACTICE OF MEDICINE. 

vious attacks of chorea. The general nutrition of the 
child should be maintained, and anaemic conditions should 
promptly be met by the administration of iron and arsenic. 
For the attack itself rest and seclusion constitute important 
elements in the treatment, and are insisted upon by Osier. 
The child should be put to bed and kept quiet until the 
movements have ceased. By this procedure the liability to 
heart complication is materially diminished. The child 
should be kept quiet, and should not be excited by toys or 
by seeing too many people. The diet should be nourishing 
and abundant. Arsenic is the best form of medicinal treat¬ 
ment, and is given as a matter of routine practice. Chil¬ 
dren bear the drug well. Fowler’s solution is to be given 
in 3-minim doses well diluted, after meals; the dose should 
be increased by 2 minims every second or third day until 
from 12 to 15 minims are taken at each dose. Should toxic 
symptoms appear—vomiting, diarrhoea, itching of the eye¬ 
lids, oedema, or skin affections—the drug should be stopped 
for three or four days and then be resumed at the same 
dose as that last taken. According to Osier, arsenic seems 
to exert no specific action upon the disease, but does good 
by improving the general condition. 

Of other remedies, cimicifuga, chloral, sulphonal, physo- 
stigmine, antipyrine in 20- to 60-grain doses throughout 
the day, and quinine in large doses have been recommended. 
The zinc compounds, strychnine, and sodium bromide may 
also be tried in obstinate cases. Iron is required in nearly 
all cases to combat anaemic conditions. 

For chorea insaniens hydrotherapy, in the form of the 
wet pack or the bath, should be tried, and the patient 
should be quieted by chloral, morphine, or, in the severest 
cases, by whiffs of chloroform. The cardiac affections are to 
be treated on general principles. Obstinate cases may be 
benefited by change of air and by enforced rest and seclusion. 


CHOREA. 


879 


Choreiform Affections. 

Habit-spasm (Habit-chorea; Simple Tic).—This condition 
is common in childhood, and may persist during life. The 
patients are frequently over-grown children of a neurotic 
personal or family history. There may be twitching of the 
eyelids, facial grimaces, shrugging of the shoulders, or short 
inspiratory sniffs. In severer forms nearly all the muscles 
of the face are affected. A “ generalized tic ” occurs in 
children and in adults and may persist for years. The 
muscles of the extremities and of the trunk suddenly jerk, 
producing the effects of a general electric contraction 
(“ electric chorea ”). 

Tic Convulsif (Gilles de la Tourette’s Disease).—In this 
form which usually occurs in nervous children with a neur¬ 
otic family history, in addition to motor spasms there 
occur explosive utterances of sounds or of words. A 
sound may be repeated over and over again ( echolalia ), or 
obscene and profane words may be used {coprolalia). In 
some cases fixed ideas are present; of these, arithniomania 
is the most common, in which condition the patient feels 
obliged to count a certain number of figures before almost 
every action. 

Huntingdon's Chorea (Chronic Chorea).—This rare disease 
is characterized by its hereditary nature, a tendency to 
insanity and suicide, and its late onset between the thirtieth 
and fortieth years. When one or both parents have been 
subject to the disease, one or more of the offspring invari¬ 
ably become affected ; but the hereditary character of the 
disease is peculiar in that it never skips one generation to 
manifest itself in another. The pathology of the disease is 
obscure. 

The symptoms are first manifested in the hands by irreg¬ 
ular movements; later the movements are disorderly and 


880 MANUAL OF THE PRACTICE OF MEDICINE. 


inco-ordinate, and have not the jerky character of the true 
choreic contractions. Slow involuntary facial grimaces 
occur; the gait becomes swaying and irregular, and has 
been aptly compared to that of a drunken man. The arms 
and hands are usually in more or less constant irregular 
motion. The speech is affected in the majority of cases, 
becoming slow, hesitating, and indistinct. Mental impair¬ 
ment becomes progressively marked, and ultimately termi¬ 
nates in dementia. 

TETANY; TETANILLA. 

Etiology. —This condition, which is rare in the United 
States, most commonly occurs before the twentieth year. 
In the great majority of cases an exciting cause can be dis¬ 
covered—exposure to cold, acute diseases, especially typhoid 
fever, fatigue, lactation (“nurse’s contracture”), or preg¬ 
nancy. In young children the indications of rickets are 
seldom absent. Tetany occurs in about one-sixth of the 
cases of removal of the thyroid gland, and may be fatal. 
Epidemics of tetany are described as occurring on the 
Continent of Europe, and appear to be due to some un¬ 
known infection. A rare but fatal form complicates dilata¬ 
tion of the stomach. 

The pathology of the disease is unknown. It is prob¬ 
able that the disease depends upon the action of some toxic 
agent upon the motor centres. 

Symptoms.—The spasms are bilateral, and begin in the 
hands and feet. The fingers are flexed at the metacarpo¬ 
phalangeal joints, extended at the others ; the thumb is 
flexed and adducted; the palm is hollowed. The wrist is 
flexed, and the arm may be folded over the chest. The feet 
are extended and inverted ; the toes are flexed. In severe 
cases the muscles of the trunk and of the face may be 
involved, and there may be trismus. Dyspnoea and cyano- 


TETANY; TETANILLA . 


881 


sis may result from spasm of the respiratory muscles. The 
spasms are usually paroxysmal, lasting from several minutes 
to several hours or even days, but in some severe forms the 
symptoms are continuous for several weeks. In the acute 
forms there may be a moderate fever, a feeling of “ pins- 
and-needles ” in the hands, and a cramp-like pain in the 
affected muscles. During the height of the paroxysm, and 
persisting for several weeks afterward, there is a greatly 
increased excitability of the affected nerves to the galvanic 
and the faradic current, tetanic contractions following the 
application of a current which in health would produce no 
appreciable reaction. The slightest tap on the affected 
muscle causes also a conspicuous contraction. The cha¬ 
racteristic spasm may also be induced by pressure on the 
artery, sometimes by pressure on the nerves of the limb 
(“Trousseau’s phenomenon”). 

Diagnosis.—From tetanus the disease is distinguished by 
the fact that the earliest symptom in tetanus—trismus—is 
the latest in tetany. Hysterical contractures are almost 
invariably unilateral, while tetany never is. Cases of carpo¬ 
pedal spasms in rickety children should not be regarded as 
cases of true tetany. 

The prognosis is favorable except in those cases following 
thyroidectomy or dilatation of the stomach. Future attacks 
are liable to occur, however, if the exciting cause be repeated. 

Treatment.—The cause of the disease should be traced 
and removed. Lactation should be stopped, and in all cases 
a tonic form of treatment, with baths and cold sponging, 
should be advised. Sodium bromide relieves the spasm 
most effectively, but cannabis indica or chloral may also be 
used. Ice to the spine has been recommended. Electrical 
treatment is disappointing. Faradism is contraindicated. 
Massage under chloroform-narcosis has been followed by 
good results in obstinate cases. 

56 


882 


MANUAL OF THE PRACTICE OF MEDICINE. 


MIGRAINE. 

Etiology and Synonyms.—This affection, which is often 
inherited, is more common in women and in members of 
neurotic families. In many of the cases there is a history 
of rheumatic or gouty taint. The existing cause may be 
mental or bodily fatigue, emotions, indigestion, or the eating 
of some particular article of food. Among reflex causes 
should be mentioned uterine disease, eye-strain, abnormal 
conditions of the nose or of the naso-pharynx, and carious 
teeth. A reflex source of irritation should always be 
suspected in the migraine of young patients. The attacks 
often appear with striking periodicity, and usually cease 
after the climacteric, or in men after the fiftieth year. 
Synonyms: Hemicrania; Sick headache. 

Pathology.—The nature of the disease is unknown. 
Liveing’s theory is that it is a nerve-discharge from sensory 
centres—the sensory equivalent of epilepsy; according to 
others the disease is a vaso-motor neurosis. 

Symptoms.—Premonitory symptoms are present in 
many cases. There may be malaise, lassitude, and a 
sense of chilliness. Visual prodromes are not uncom¬ 
mon—hemianopia, spots of dimness of vision or scoto¬ 
mata, apparitions, balls or flashes of light, and zigzag 
lines. Sensory prodromes consist in numbness or tingling 
of a hand or an arm, or of peculiar sensations in any part 
of the body. There may be a condition of intense emo¬ 
tional activity. Motor prodromes consist in temporary 
weakness of certain groups of muscles or of aphasia. 

The prodromal symptoms are not always present. In 
some cases they may comprise the entire attack, not being 
followed by headache. 

The characteristic symptom of migraine is the violent 
paroxysmal headache. 


MIGRAINE. 


883 

beginning over one side, usually most intense over the 
frontal legion or over the eye, the pain grows more and 

more unendurable. In rarer instances the headache is 
bilateral. 

The pain is usually described as of a sharp, boring cha- 
lacter, and is regularly increased by the slightest sound or 
light. Prostration, though temporary, is extreme. During 
the early part of the attack the face may be pale and 
pinched, and there may be a marked difference between its 
two sides. Subsequently the face becomes flushed from 
vaso-motor dilatation. During the attack there is usually 
mental confusion, or even temporary loss of memory. The 
pulse may be slow and the temporal artery contracted and in 
a condition of arterio-sclerosis. When the headache reaches 
its climax nausea and vomiting commonly appear j the 
vomiting generally affords relief, so that the patient may 
fall at once into a sound sleep and awake refreshed. 

The duration of an attack varies from several hours to 
several days. 

Migraine is not accompanied by fever except in chil¬ 
dren, in whom a temperature of 102° to 103° F. may be 
developed. 

Prognosis.—Much can be done to render the attacks less 
frequent and severe, but the disease cannot be radically cured 
by medication. Spontaneous cure usually occurs between 
the fortieth and fiftieth years. 

Treatment.—Each patient is usually aware of the causes 
that precipitate an attack, and if these causes be avoided 
the paroxysms are rendered much more infrequent. Periph¬ 
eral irritations, such as eye-strain, nasal hypertrophies, or ade¬ 
noid growths in the naso-pharynx, require appropriate treat¬ 
ment. Attacks of migraine become infrequent during good 
health; the patient therefore should be built up, and gouty 
and rheumatic tendencies should be corrected. During the 


884 MANUAL OF THE PRACTICE OF MEDICINE. 

paroxysm the patient should be put to bed and kept abso¬ 
lutely quiet. A small cup of strong hot coffee frequently 
affords relief. Much benefit is derived from the use of 
antipyrine or phenacetine, especially when given in small 
repeated doses. If there be conspicuous pallor, nitroglycerin 
in does of gr. T fg- may be given every two hours. Can¬ 
nabis indica (gr. Herring’s English Extract), sodium 
bromide (gr. xxx), and chloral hydrate (gr. x—xv) are all 
of service. A prolonged course of cannabis indica is fre¬ 
quently beneficial in reducing the number of attacks. 
Of other remedies, caffeine, guarana, ergot, and sodium 
salicylate have been recommended. 

OCCUPATION-NEUROSES. 

Etiology.—Certain localized motor affections occur in 
those whose occupation requires the constant repetition of 
complicated muscular movements. The most common 
form is “ writer’s cramp,” but piano- and violin-players, 
telegraphers, and cigarette-rollers may be similarly affected. 
Men are more frequently attacked than women. Predispo¬ 
sition is afforded by any of the causes leading to neuras¬ 
thenia. 

Pathology.—The condition is one of local neurasthenia, 
the affected nerve-centres being in a condition of “ irritable 
weakness.” 

Symptoms.—The principal symptoms are pain and 
spasm. A paralytic form has also been described. The 
symptoms of “ writer’s cramp” may be taken as a type. 
There is a feeling of fatigue in the affected muscles, amount¬ 
ing to actual pain when writing is attempted; tremor and 
irregular spasmodic contractions occur, rendering the writ¬ 
ing illegible; later the pain may be more continuous, may 
spread over the arm, and may be accompanied by tender¬ 
ness along the course of the nerve-trunks. 


NEURASTHENIA. 885 

The prognosis must be made guardedly, as the condition 
tends to become chronic, and even when relieved by treat¬ 
ment the affection is liable to recur. 

Treatment. —It is important that in writing the motions 
should be made from the arm or the forearm, and not from 
the wrist or the little finger, as the fixed point. When the 
symptoms are first noticed rest is imperative. The various 
devices of complicated pen-holders only serve to stave off 
the disability and allow the patient to do his work while the 
malady is really getting worse. Massage and systematic 
gymnastics are of service. Electricity does not seem to do 
good. No form of treatment, however, is of benefit that is 
not combined with rest. The general nutrition of the 
patient should be improved in every way. Nervine tonics, 
as phosphorus and strychnine, are to be recommended. 

NEURASTHENIA. 

Etiology. — Nervous weakness and irritability occur 
when the expenditure of energy exceeds its supply. The 
following classification of causes is given by Starr : 

A. Excessive expenditure of nerve-energy (primary neuras¬ 
thenia): (1) Bad hereditary influences, weak nervous sys¬ 
tem ; (2) feebleness in childhood, with poor nervous system ; 
(3) wrong methods of training; (4) the struggle for exist¬ 
ence; (5) anxiety, mental depression, worry, fear; (6) men¬ 
tal or physical over-work ; (7) sexual excesses. 

B. Deficient supply of nervous energy (secondary neuras¬ 
thenia): (1) Weakening diseases of all kinds, of an organic 
nature; (2) indigestion and dyspepsia, with auto-infection 
by toxic products; (3) gout, rheumatism, uric-acid diathe¬ 
sis; (4) infectious diseases—typhoid, grippe, malaria; (5) 
alcoholism and the abuse of drugs. 

Pathology. —There are no anatomical lesions. The con¬ 
dition consists of “ irritable weakness ” of the nervous centres. 


886 MANUAL OF THE PRACTICE OF MEDICINE. 


The symptoms of neurasthenia are so varied that only a 
brief description can be given of the important manifesta¬ 
tions of the disease. The various symptoms are grouped 
in patients in an infinite variety of combinations. 

Cerebral and Mental Symptoms. —There is an inability to 
perform the ordinary mental work. The patient is moody, 
apprehensive, irritable, and depressed, and complains of a 
sense of fulness in the head, of throbbing, or even of actual 
headache. Suboccipital headache is common, and is usually 
associated with insomnia. The eyes are easily tired after 
reading for a few minutes. 

Spinal Symptoms. —There are weariness on exertion, pain 
in the back, and tender spots along the spine. Pain over 
the cervical vertebrae and the sacrum is not uncommon. 
Sexual neurasthenia is characterized by nocturnal emis¬ 
sions, impaired power, and a distressing dread of impo¬ 
tence. 

Vaso-motor symptoms consist of hot and cold flashes, 
localized sweatings, transient blueness, or oedema. Palpita¬ 
tion, irregular heart-action, and painful feelings in the heart 
are commonly present, and distress the patient with the 
belief that he has serious organic disease of the heart. 
Tachycardia may occur. 

Gastro-intestinal Symptoms. —There may be nervous dys¬ 
pepsia, or hyperacidity, or hypersecretion. Constipation is 
the rule. There may be membranous colitis, especially 
in women. Tympanites is a common symptom. Gastro¬ 
intestinal neurasthenia is often associated with dilatation of 
the stomach and floating kidney, the combined conditions 
being termed “ enteroptosis.” 

Urinary Symptoms. —In many cases oxalate of lime or 
uric acid is present in the urine—the so-called “ lithaemic 
neurasthenia.” There may be polyuria. 

The diagnosis is made by the grouping of a variety of 


HYSTERIA. 


887 


neurasthenic symptoms without actual organic disease. In 
many cases the diagnosis is rather a question of medical 
intuition. 

The prognosis is good if the exciting cause can be 
removed and if the patient is in such a financial condition 
as to be able to carry out the necessary treatment. Many 
patients, handicapped from birth with a weak nervous 
system, do well only when no demands are made upon 
their strength; as soon as any emergency arises they go 
under. 

Treatment.—The most important indication is to dis¬ 
cover the cause; this often requires an intimate and personal 
knowledge of each individual patient. Over-worked busi¬ 
ness-men are best treated by rest with a change of scene, as 
by a trip abroad. Pleasant physical exercise to the point 
only of moderate fatigue is often beneficial. The general 
nutrition should be improved in every way by proper food, 
sufficient sleep, and a proper amount of recreation, and by 
massage, hydrotheraphy, and tonics. The drug treatment 
of these patients should be limited, however, as much harm 
is done by over-dosing. Stimulants and narcotics are to be 
withheld, as habits are easily formed. In severe cases the 
Weir-Mitchell rest-cure may be recommended. 

HYSTERIA. 

Etiology.—This most perfect type of a functional malady 
is the product of advanced civilization. Unknown among 
barbarous nations, it reaches its highest development among 
the French people. Hysteria is twenty times more common 
in women than in men, and usually appears between the 
ages of fifteen and twenty, although manifestations may con¬ 
tinue until late in life. In many cases there is a family his¬ 
tory of nervous troubles. With or without such an inherited 
neurotic predisposition, hysteria may be induced by injudi- 


888 MANUAL OF THE PRACTICE OF MEDICINE. 


cious training, an unstable moral organization, or a lack of 
self-control. Among more direct influences are emotions, 
unhappy love-affairs, domestic worries, sexual excess, 
masturbation, and physical enfeeblement by injury or acute 
disease. In some cases ovarian or uterine disease seems 
capable of originating hysteria, but these cases are much 
less common than are ordinarily supposed. Hysterical 
symptoms may spread to other patients by sympathetic 
imitation, or “ moral contagion ” as it may be termed. 

Pathology. —There is no organic lesion in hysteria ; the 
condition is entirely functional. 

Symptoms. —The clinical picture of hysteria is so varied 
and complex that only a brief description of individual 
symptoms can here be given, and no attempt will be made 
to evolve a general picture of the disease. 

i. Motor Symptoms. — (a) Convulsive Seizures .—A mild 
and a severe form of hysteria are recognized. The mild 
form usually appears after emotions. The patient becomes 
“ hysterical,” laughs and cries alternately, and complains 
of a constricted feeling in the throat, as if a ball were rising 
into it (“ globus hystericus”). There may even be painful 
sensations, referred to some internal organ, resembling 
sensory aurae. The patient then falls into convulsions, but 
not as suddenly as in epilepsy. The convulsive movements 
are clonic and irregular. The attack subsides gradually, 
usually with the passage of flatus or of a large quantity of 
limpid urine, and the patient, as a rule, has no recollection 
of what has happened. 

The severe form, or hystero-epilepsy, is not as common 
in America as in France. The convulsions, which are 
usually preceded by minor hysterical manifestations, simulate 
true epileptic attacks; but they last longer, the tongue is not 
bitten, and the movements are not shock-like. The convul¬ 
sive seizure is usually followed by emotional displays, by 


HYSTERIA. 


889 

cataleptic poses, by opisthotonos or other distortions, and by 
attitudes and grimaces expressive of the deepest emotions. 
As the patient emerges from the condition delirium and 
hallucinations are not uncommon, or the patient may sink 
into a prolonged trance. The attacks may frequently be re¬ 
peated, as in the status cpilepticus , but, unlike that condition, 
do not seem to exert a deleterious effect upon the general 
health. 

( b ) Paralysis is common and may involve any part of the 
motor apparatus. The onset may follow a convulsive 
seizure or may be induced by emotion. The paralysis may 
be hemiplegic, paraplegic, or monoplegic. Hemiplegia is 
more common upon the left side, and is usually associated 
with hemiansesthesia. The face is not affected. Hysterical 
paraplegia is the most common form of paralysis, and the 
affected muscles may be flaccid or spastic. There may be 
only loss of power for certain combined movements (as 
walking), while the patient still retains the power to move 
the legs in bed. The reflexes may be increased, there is 
irregular voluntary resistance to passive motion, and a 
spurious ankle-clonus may be present. The muscles do not 
waste, the electrical reactions are normal, and bed-sores do 
not occur. The feet are usually extended and inverted. 
In some cases ataxia occurs, with paresis. Other hysterical 
manifestations are usually combined with paresis, forming 
a more or less characteristic symptom-complex. A charac¬ 
teristic form of hysterical paralysis is aphonia, in which the 
voice is lost or reduced to a whisper. Examination shows 
lack of approximation of the vocal cords during phonation, 
although the glottis can readily be closed by coughing. In 
many cases hysterical aphonia complicates acutt. catarrhal 

laryngitis. 

(c) Contractures and Spasms— Contractures may be hemi¬ 
plegic, paraplegic, or monoplegic in type. The smaller 


89O MANUAL OF THE PRACTICE OF MEDICINE. 

joints are usually flexed, the larger joints extended. Ankle- 
clonus, exaggerated reflexes, and a spastic gait are com¬ 
monly present, so that the case may resemble lateral scle¬ 
rosis so closely that a differential diagnosis may be impos¬ 
sible. The contractures disappear, however, during sleep 
and during chloroform-narcosis, and, although usually pro¬ 
tracted, tend eventually to disappear spontaneously. Hys¬ 
terical trismus is not uncommon. Contractures of certain of 
the abdominal muscles, combined with relaxation of the recti 
and the inflation of the intestines with gas, produce “ phan¬ 
tom tumors,” which in some instances are associated with 
the symptoms of spurious pregnancy or even of labor. 
Phantom tumors readily disappear under full anaesthesia. 

Clonic spasms are not uncommon, and are generally 
rhythmic in character (“ rhythmic chorea,” “ hysterical 
chorea”). Volitional tremor may exist, resembling that of 
insular sclerosis. 

2. Sensory Symptoms. — (a) Anesthesia is exceedingly com¬ 
mon, occurring usually in irregular areas which may also 
be insensitive to touch and devoid of the muscular sense. 
Hysterical hemianaesthesia is so characteristic as to possess 
positive diagnostic value. 

(/;) Hyperesthesia may give rise to spontaneous pain, or 
merely to tenderness upon palpation. Hyperaesthetic areas 
are rare on the extremities, but are common on the head, 
especially over the sagittal suture. This pain over the 
vertex, of an agonizing character, is likened to the pain 
which would be experienced if a nail were being driven 
into the head, hence the term claims hystericus which has 
been applied to it. Other hyperaesthetic areas are com¬ 
monly found over the sternum, under the mammae, along 
the vertebral column, and over the ovaries. If pressure 
applied to these hyperaesthetic zones induces hysterical mani¬ 
festations, the zones are frequently spoken of as “ hystero- 


HYSTERIA, 


89I 


genic points.” Spinal hyperesthesia may affect the whole 
column or only a single segment, and is often so ex¬ 
treme that the slightest touch gives rise to exquisite pain. 
Abdominal hyperesthesia may simulate gastric ulcer, ap¬ 
pendicitis, or peritonitis. In the latter case the resemblance is 
almost perfect, even to the presence of fever and the perito¬ 
neal facies. Hypersesthesia of the breast may be accom¬ 
panied by a diffused swelling of the gland, but the hysterical 
breast may be recognized by the exquisite superficial ten¬ 
derness, by constant variations in the swelling, and by the 
recurrence of the symptoms at the menstrual period or after 
exceptional excitement or fatigue. 

3. Special Senses .—There may be limitation of the visual 
field, especially for colors, or there may be hemianopia. 
The color-sense may be partially or completely lost (hyster¬ 
ical achromatopsia). Loss of the senses of smell and taste are 
not uncommon. Hysterical deafness may occur alone or 
may alternate with attacks of hysterical blindness. Hyper- 
aesthesia of the eye or the ear may also occur, the former 
being the more common. 

4. Digestive Symptoms .—The globus hystericus, or the feel¬ 
ing as though a ball were rising in the throat, may be asso¬ 
ciated with pharyngeal spasm. The spasm may spread to 
the oesophagus, so that swallowing becomes difficult or im¬ 
possible (see Spasmodic Stenosis of the CEsophagus). Hys¬ 
terical vomiting, in which the food is regurgitated soon after 
eating, and without attendant nausea, may persist for months 
without marked failure in nutrition. An antagonism to food 
(>hysterical anorexia , or anorexia nervosa) may occur in young 
girls, and may be so marked that no food is taken for days; 
the patient finally becomes emaciated to an extreme degree, 
and death from asthenia may result in rare instances. De¬ 
ception, however, is practised in the vast majority of these 
“ fasting girls,” food being taken unobserved. Depraved appe- 


892 MANUAL OF THE PRACTICE OF MEDICINE. 

tite, dyspepsia, and gastric pains are not uncommon. Peri¬ 
staltic unrest (see page 479) may also occur. Reversed peri¬ 
stalsis has occurred, the patient vomiting rectal enemata that 
have been previously given. Flatulency is common and dis¬ 
tressing. Nervous diarrhoea may occur, diarrhceal move¬ 
ments usually being induced by eating. Constipation is 
more frequent, and may be so obstinate in character that the 
bowels do not move for weeks, despite energetic medication. 
Haematemesis due to vaso-motor disturbance may undoubt¬ 
edly occur, but in every case deception should be suspected. 

5. Respiratory Symptoms .—Rapid breathing (50 to 120 to 
the minute), without increased frequency of the pulse or other 
symptoms of dyspnoea, is characteristic of hysteria. Actual 
dyspnoea may attend laryngeal spasm, and suffocation may 
seem imminent. Hysterical aphonia has already been al¬ 
luded to. Extraordinary cries and sounds, resembling those 
produced by animals, may be emitted. A dry, paroxysmal 
barking cough is a frequent symptom in chlorotic girls, and 
may spread in schools by unconscious imitation. Spurious 
haemoptysis may occur, the sputum being usually pale-red 
in color rather than the crimson color seen in true hem¬ 
orrhage. In these cases the blood comes from the mouth 
or the pharynx. In other cases deception is practised. 

6. Circulatory Symptoms .—Cardiac irritability, palpitation, 
and pain over the heart are common symptoms. The car¬ 
diac pain may give rise to the symptoms of pseudo-angina 
pectoris. Hot and cold flashes, pallor, and flushings with a 
sensation of heat result from vaso-motor disturbance. 
Localized flushings, areas of circumscribed oedema, and 
similar phenomena may occur. Stigmata, or hemorrhages 
in the skin, may occur, although in the vast majority of 
cases they are of fraudulent origin. 

7. Urinary Symptoms .—After hysterical manifestations 
the urine is abundant, limpid, and of a low specific gravity. 


HYSTERIA. 


*93 


Retention of urine is common; incontinence is unknown. 
The urine may be partially or completely suppressed, and 
this hysterical anuria may last for days, during which time 
the sweat, vomit, and other secretions become loaded with 
urea. It is a characteristic of hysterical anuria that uraemic 
symptoms do not appear. Irritation of the bladder, shown by 
a constant desire to pass urine, is a frequent and trouble¬ 
some symptom. 

8. Joint-symptoms (Brodies Joint).—The larger joints, 
especially those of the knee and the hip, are usually affected, 
and the symptoms may follow slight injuries. The joint is 
swollen, resists passive motion, and is flexed, although 
changes in position occur from day to day. The skin over 
the joint is hyperaesthetic and usually cool, but heat may be 
observed, especially at night, accompanied with pain. Motion 
and handling are painful. In protracted cases the muscles 
about the joint may waste. In rare instances organic 
changes in the joint may succeed the functional disturb¬ 
ance. 

9. Temperature .—In hysteria the temperature is usually 
normal, although in severe cases a slight rise may be ob¬ 
served. Rare cases of “ hysterical fever ” are reported, in 
which a periodic elevation of temperature to 102° or 103° 
F. has been recorded. In very exceptional cases a rise to 
108 0 or iio° F. has been noted, but these high tempera¬ 
tures are in all probability fraudulent. Cases of hysterical 
fever with spurious local manifestations are most deceptive. 
The occurrence of fever with hysterical symptoms resem¬ 
bling peritonitis has been described. Fever with pain in 
the head, photophobia, contracted pupils, vomiting, and 
retraction of the neck may closely resemble meningitis. 

10. Mental Symptoms .—There is usually an exaggeration 
of ordinary emotional excitement. The moral character 
becomes changed; the patient becomes low-spirited and 


894 MANUAL OF THE PRACTICE OF MEDICINE. 

listless or inquisitive and fussy. Often the patient’s attention 
is morbidly concentrated upon herself. Whims of the 
most varied kind are invented from time to time; the 
patients show a marked tendency to deceive others, evince 
a wish to become objects of notoriety, and not the slightest 
dependence is to be placed upon their statements. Other 
patients become sullen and refuse to answer questions. 
Attacks of insanity and persistent hallucinations and de¬ 
lirium may occur. Trance or catalepsy may develop. 

Prognosis.—The danger to life is so extremely small 
that it may be disregarded. The duration varies according 
to the severity of the symptoms, the moral force of the 
patient, the duration of the operative cause, and the home 
surroundings and environment. 

Treatment.—It is essential that the physician should 
gain the patient’s confidence from the start, and that he 
should enter into every detail of her daily life, so as to dis¬ 
cover what elements are at work perverting her nervous 
forces. Hysteria arising from an unhappy home-life, from 
disappointments in love, and from kindred causes is best 
treated by travel and total change of environment. In 
many cases routine employment is to be recommended. 
The physician should not forget that the patient’s complaints 
are not entirely imaginary, but that the suffering often is 
real. On the other hand, too much sympathy should not 
be given by either physician or friends. Many patients im¬ 
prove at once when they are taken from fussy and solicitous 
relatives and placed among strangers, where self-control 
must of necessity be exerted. 

The general health must be improved in every possible 
way. The diet should be wholesome and abundant; exer¬ 
cise should be graded; and sufficient hours for rest and 
sleep must be insisted upon. Laxatives and other medica¬ 
tion are indicated should dyspeptic symptoms be present. 









SUN-STROKE . 


895 


Bromide of sodium, phenacetine, valerian, asafcetida, and 
similar antispasmodic drugs are of service during the acute 
manifestations of the disorder, but the continuous use of 
these remedies as a routine treatment is much to be de¬ 
plored. Morphine should never be used. 

In severe and intractable cases the Weir-Mitchell rest- 
cure—a combination of seclusion, rest, and forced-feeding— 
may be recommended, especially for under-nourished 
patients with marked hysterical manifestations, and for 
those who are constantly passing over the limits of their 
nervous strength. A bright, intelligent nurse and a com¬ 
plete isolation from family and friends are essential features 
of this treatment. Rest in bed for three or four weeks, 
with daily exercise of the muscles by faradism or massage, 
usually allows the strained nervous system to return to its 
normal condition and improves body-nutrition. The diet 
during the first ten days is to be milk alone; later, solid 
food is to be added gradually. 

For hysterical vomiting and anorexia nervosa forced feed¬ 
ing by the stomach-tube is to be employed. During a con¬ 
vulsive attack a cold douche may be applied to the head, 
with the assurance to the family, in the hearing of the 
patient, that there is no danger, but that the cold applica¬ 
tions will be continued until relief is experienced. In 
many instances, however, it is better to leave the patient 
alone and unnoticed until the attack subsides spontaneously. 
The treatment of hysterical paralysis by hypnotic sugges¬ 
tion has occasionally been followed by brilliant results. 

SUN-STROKE. 

Two distinct conditions due to exposure to intense heat 
are encountered—heat-exhaustion and thermic fever. 

Heat-exhaustion may be induced by exposure to the 
hot sun or to any great artificial heat, as in engine-rooms. 


896 MANUAL OF THE PRACTICE OF MEDICINE. 

There is prostration bordering upon collapse; the skin is 
cool and clammy; the face is pale; the pulse is rapid and 
feeble; the temperature is regularly subnormal. The onset 
of symptoms may be gradual, or may be so abrupt that the 
patient will fall in syncope. In severe cases the conscious¬ 
ness may be lost and muttering delirium may occur. It is 
thought that the condition is dependent upon a vaso-motor 
paresis as the result of which there is a determination of 
blood from the surface of the body and the brain to the 
large abdominal blood-vessels. 

Treatment.—External heat should be applied, preferably 
by the hot bath. Stimulants should be freely administered. 

Thermic Fever (Sun-stroke; Heat-stroke; Insolation; 
Coup de Soleil).— Etiology. —This condition is most fre¬ 
quent when great heat is combined with a high percentage 
of humidity. Excessive bodily fatigue and intemperance 
are predisposing factors. 

Pathology.— Rigor mortis occurs early, and putrefactive 
changes appear rapidly. The blood is dark and imperfectly 
coagulated. There are parenchymatous changes in the 
liver and kidneys. The lungs are intensely congested. 

The symptoms may begin abruptly, the patient falling 
unconscious to the ground ; or they may be preceded by 
pain in the head, nausea and vomiting, vertigo, dimness of 
vision, or colored vision. When first brought under observa¬ 
tion the patient is unconscious, with deep stertorous breath¬ 
ing and a rapid bounding pulse. The carotid arteries 
pulsate visibly. The skin is hot, dry, and reddish. Urine 
and feces are usually discharged involuntarily. The eyes 
are suffused, the pupils are variable, sometimes contracted, 
sometimes dilated. The temperature varies between 106° 
and 112 0 F., the average maximum height being about 
108 0 F. Convulsions, muscular rigidity, and temporary 
delirium of an active form are of common occurrence. If 





SUN-STROKE. 


89 7 

the patient is to do badly, the pulse becomes rapid and 
iiregulai, the breathing becomes irregular or “ Cheyne- 
Stokes,” and death 


109h 



oc¬ 
curs, usually within from 
twenty to thirty-six hours. 

In very severe cases coma 
and heart failure may cause 
death within a few hours; 
in rarer cases instantane¬ 
ous death may occur. 

A mild form of heat- 
fever, which occurs in 
tropical countries and gives 
the symptoms of a con¬ 
tinued fever resembling ty¬ 
phoid, has been described 
under the terms “ ardent 
continued fever” and 
“ thermic continued fever.” 

Sequela consist of (1) inability to bear exposure to heat 
without headache and distress; (2) pain in the head, that 
may be constant for months; (3) mental weakness with 
nervous irritability. In rarer cases insanity or chronic 
meningitis may result. 

The prognosis is grave. About one-third of the cases 
end fatallv. 

Treatment.—Immediate reduction of the body-tempera¬ 
ture is most urgently indicated. Cold affusions and appli¬ 
cations of ice to the surface must be resorted to without 
delay. When practical, the cold bath (50° to 6o° F.) should 
be given; ice-water enemata may be serviceable. When a 
bath cannot be secured, the value of an ice-pack cannot be 
over-estimated. The cold applications are to be continued 
until the temperature is well under control. Internal anti- 
57 





























































8g8 MANUAL OF THE PRACTICE OF MEDICINE. 


pyretics are not as serviceable as cold hydrotherapy. In 
very severe cases free venesection may be resorted to. In 
convulsions and delirium, morphine is to be given hypo¬ 
dermically. Stimulation is required in the majority of cases. 

DELIRIUM TREMENS. 

Etiology and Synonym.—Delirium tremens may be in¬ 
duced in hard drinkers by excesses, by sudden withdrawal 
of liquor, by fright, shock, or acute inflammation, especially 
pneumonia. Synonym : Mania a potu. 

Symptoms.—The patient becomes tremulous, nervous, 
and is unable to sleep. Mental depression is extreme. 
After from one to three days the patient passes into the 
characteristic delirium, with visual and auditory halluci¬ 
nations of a frightful character. The temperature ranges 
between 102° and 103° F.; the pulse is rapid and soft; 
tremulousness is often so extreme as to render speech inco¬ 
herent; insomnia continues, so that the patient will get no 
sleep for three or four days. The condition either subsides 
in three or four days, especially after an induced sleep, or the 
insomnia persists, the pulse becomes more rapid and feeble, 
the delirium becomes of a low, muttering type, and death 
takes place from asthenia in a typhoid condition. Pulmon¬ 
ary congestion and oedema may complicate fatal cases. 

Diagnosis.—It is important in every case to exclude 
local inflammations, especially of the lung, that may have 
been the exciting cause for the outbreak of the delirium. 
A careful examination of the lungs should be made every 
day, as delirium tremens may be simulated by the delirium 
of pneumonia at the apex of the lung. 

The prognosis is generally good, only about 10 per cent, 
of the cases being fatal. Recurrences are to be expected 
unless the patient abandons the alcohol habit. Delirium 
tremens complicating pneumonia usually runs a fatal course. 







RAYNAUD'S DISEASE. 


899 


Treatment.—The great object of treatment is to procure 
sleep and to support the patient’s strength. The moderate 
use of opiates is recommended, but large doses are injurious. 
Alcohol should not be entirely withdrawn until after conva¬ 
lescence is established. Hydrotherapy is of service in many 
cases in controlling the delirium. Hyoscine in gr. doses 
hypodermically is of service in producing sleep. The com¬ 
bination of bromide of sodium, chloral, and tinctures of dig¬ 
italis and capsicum is used in many hospitals, as in the 
following: 

3 ^. Chloral hydrate, 

Sodium bromide, 

Tinct. digitalis, 

Tinct. capsici, 

Spir. amnion, aromat., 3j ; 

Aquae, q. s. ad 3ij.—M. 

Sig. Dose every two to three hours. 

The patient should be constantly guarded by attendants 
night and day, to prevent his escape or injury. If necessary, 
he should be tied down by a draw-sheet, or in severe cases 
the strait-jacket may be applied. 


gr. x; 
3 ss ; 

aa. TY1 v ; 


7. VASO-MOTOR AND TROPHIC DISORDERS. 

RAYNAUD’S DISEASE. 

This vaso-motor neurosis presents three grades of inten¬ 
sity—local syncope, local asphyxia, and local or symmetri¬ 
cal gangrene. The majority of cases occur in young women. 

Local syncope , the most common form, leads to coldness 
and pallor of the extremities (“ dead fingers,” “ dead toes ”), 
and may be induced by cold or by emotions. The affected 
parts are stiff, but are rarely painful. The condition lasts 
for a variable time and may be succeeded by local asphyxia. 




900 MANUAL OF THE PRACTICE OF MEDICINE . 


Local Asphyxia .—There are lividity and cyanosis of the 
affected parts (the fingers, toes, ears, nose), with numbness, 
swelling, and some pain. The capillary circulation is ex¬ 
ceedingly sluggish. The condition may follow that of local 
syncope. As the attack wears off, the affected parts become 
bright red from over-active circulation. Severe attacks may 
be followed by local gangrene. Recurrences are common, 
especially during the winter months. 

Local or Symmetrical Gangrene .—Ecchymotic spots and 
vesicles appear, and become the starting-point for a dry 
gangrene which is usually remarkably symmetrical. The 
ears, fingers, and toes are the special seats of selection. The 
affection may be complicated by purpura haemorrhagica, 
intermittent haemoglobinuria, peripheral neuritis, and a vari¬ 
ety of mental and cerebral symptoms. 

Diagnosis.—The disease must not be confounded with 
the dry gangrene due to obliterating endarteritis. 

The prognosis is good except in the extensive forms of 
gangrene or in the gangrenous cases complicated by pur¬ 
pura haemorrhagica. 

Treatment.—Exposure to cold should be avoided, and, 
if possible, the patient should spend the winters in a warm 
climate. The continuous electrical current may be applied 
to the spine and the extremities. Internal medication seems 
to exert no beneficial effect upon the disease. 

\ 

ACUTE CIRCUMSCRIBED CEDEMA. 

Etiology and Synonyms.—This disorder, which is often 
of a distinctly hereditary character, may be induced reflexly 
by gastric disorders. Attacks occur in some instances with 
remarkable periodicity. Nothing further is known of its cau¬ 
sation. Synonyms : Angio-neurotic oedema ; Giant urticaria. 

Pathology.—There is a localized vaso-motor dilatation 
allowing of the transudation of serum. 


FACIAL HEMIATROPHY. 


901 


Symptoms.— A circumscribed oedematous swelling oc¬ 
curs in some part of the body, more commonly on the 
face or the arms. The skin is pale and tense, but there 
may be redness of the integument resembling that of an 
inflammatory swelling. Itching and burning sensations 
usually accompany the outbreak. There may be sudden 
and fatal oedema of the glottis. Gastro-intestinal symptoms 
—nausea and vomiting, very severe abdominal pain, and 
diarrhoea—usually accompany the attacks. Urticaria may 
precede the outbreak. 

The prognosis is good unless the larynx be involved, but 
recurrences are the rule. 

Treatment. —A general tonic treatment is usually indi¬ 
cated, and indigestion and over-eating must be avoided; 
otherwise the treatment is unsatisfactory. 

FACIAL HEMIATROPHY. 

Etiology and Synonym.— This rare condition occurs 
more often in men than in women, and is rare after the 
twenty-fifth year. Synonym: Progressive unilateral facial 
atrophy. 

The pathology of the condition is at present undefined. 
The disease is supposed to originate from involvement of 
the trophic fibres of the fifth nerve. 

Symptoms. —A small area of atrophy begins in the skin, 
usually of the cheek or the chin, and spreads to involve 
half the face, being sharply limited by the median line. 

The deeper structures, including the bones, participate in 
the atrophy, although the muscles may undergo but little 
change. The left side of the face is the one usually in¬ 
volved. Pains and peculiar sensations may accompany the 
earlier stages of the disease, and hemiatrophy of the tongue 
and of the palate may occur. 

Prognosis. —The disease progresses slowly, and at any 


902 MANUAL OF THE PRACTICE OF MEDICINE . 


time the process may be arrested. Actual recovery does 
not occur, but the disease does not endanger life. 
Treatment is ineffectual. 

MYXCEDEMA AND CRETINISM. 

Cretinism is the infantile form of myxcedema, and is due 
to congenital absence of the thyroid gland. The symptoms 
are identical with those of the adult form of myxcedema, 

modified by the fact that 
mental development and 
body - growth are both 
arrested (see Fig. 70). 
Cretinism maybe endem¬ 
ic or sporadic. Symp¬ 
toms may appear at birth 
or during the years of 
infancy. 

Myxoedema is much 
more common in women 
than in men, and may be 
hereditary. The name 
“ myxcedema ” is derived 
from the peculiar swelling 
of the skin, due to the 
development of a myxo¬ 
matous new growth. The 
swelling is most marked 
over the face and hands, 
but may become gener¬ 
ally distributed. The skin 
and subcutaneous tissues 
are thickened, firm, re¬ 
silient, and do not pit 
on pressure. The skin is dry and rough ; the facies is cha- 



Fig. 70.—Sporadic cretinism. 





















MYXCEDEMA AND CRETINISM. 


903 


racteristic; the hair becomes coarse and falls out, and a red¬ 
dish patch is usually present on the cheeks. Physical and 
mental weakness becomes more and more marked, and may 
proceed to dementia. The speech is slow and monotonous. 
The temperature is usually subnormal. Sensory symptoms 
of a subjective nature, such as persistent unpleasant taste 
and smell, may be present. The course of the disease is 
slowly progressive, extending over years. Improvement 
under treatment, however, is to be expected. 

In myxcedema the thyroid gland is usually much dimin¬ 
ished in size, and it may become completely atrophied and 
converted into a fibrous mass. The most generally 
accepted theory is that, by reason of a failure in the function 
of the thyroid gland, certain injurious substances, which no 
longer can be rendered innocuous by the gland, collect in 
the body. 

Operative Myxcedema ; Cachexia strumipnva .—The symp¬ 
toms of myxoedema occur in animals and in men after 
removal of the thyroid gland. The condition follows only 
a certain number of complete extirpations and a smaller 
number of partial removals of the gland. Operative 
myxcedema is rare in this country. 

Treatment. —It is highly important that patients with 
myxcedema should be kept warm and be well guarded from 
cold. The winters should, if possible, be spent in a warm 
climate. Much good can be done by hot baths, friction, 
and massage. The functions of the skin should be kept 
active by jaborandi or its alkaloid pilocarpine. The essential 
treatment consists in thyroid-feeding or the use of extracts 
from the fresh thyroid glands of sheep. From one-quarter 
to one-half of a gland may be given daily, or from 2 to 5 
grains of the “ desiccated thyroid ” of any reliable maker. 
Care should be taken in ordering larger doses than these, 
as dangerous symptoms of over-dosing may ensue. 


9O4 MANUAL OF THE PRACTICE OF MEDICINE. 

SCLERODERMA; SCLEREMA. 

The causes of sclerema are unknown, although the disease 
is classed among the tropho-neuroses. The majority of 
cases occur in women of middle life. The lesion consists 
in the circumscribed or diffused production of connective 
tissue in the skin. The skin becomes hard, rigid, and ad¬ 
herent to the subcutaneous tissue. Pressure upon the 
underlying muscles may interfere with their action and 
may result in a certain amount of atrophy. Hyperaemia 
of the skin during the earlier stages may be followed by 
pigmentation or by atrophy of the pigment. The circum¬ 
scribed form of sclerema is known as “ morphoea ” or as 
“Addison’s keloid.” The diffuse form may involve large 
portions of the body, rendering motion difficult. 

The disease may develop slowly or rapidly, but when de¬ 
veloped the lesions tend to persist for months or years. 
Recovery may occur, but in most instances the disease after 
a certain length of time becomes no longer progressive. 

Massage, oil-inunctions, galvanism, avoidance of cold, and 
a tonic regimen constitute the essential points in the treat¬ 
ment. 

ACROMEGALY. 

Etiology. —Acromegaly occurs in both sexes during 
youth and middle age. The etiology of the disease is 
unknown. 

The pathology is undetermined. Hyperplasia of the 
pituitary body is an almost constant lesion, but it is also 
known that similar conditions of that structure may exist 
without acromegaly. In some of the reported cases there 
has been persistence of the thymus gland. 

Symptoms. —The hands and feet become enormously 
enlarged, owing chiefly to hypertrophy of the bones, al¬ 
though the muscles, skin, and subcutaneous tissues also 


ACROMEGAL Y 


905 


undergo hypertrophy. The nose becomes enlarged in all 
dimensions, and the lower portions of the face are strikingly 
increased in size, so that the lower jaw usually projects far 
beyond the line of the upper teeth. Hypertrophy of the 
tongue occurs in well-marked cases. The bones of the 
thorax may also become enlarged, and the back may be so 
bowed that the chin rests upon the sternum. Sensory and 
vaso-motor symptoms of varied character attend the disease, 
and there may be persistent headache. The muscular 
strength is generally poor. 

A condition allied to acromegaly has been described by 
Marie under the name of hypertrophic pulmonary osteo¬ 
arthropathy , this form being associated with pulmonary 
lesions. The condition differs from acromegaly in the fol¬ 
lowing particulars: (1) The lower jaw is not enlarged; (2) 
the articular ends of the bones are so enlarged as to interfere 
somewhat with the mobility of the joint; (3) there is a 
peculiar bulbous deformity of the terminal phalanges. 

Treatment is inoperative. 


IX. DISEASES OF THE MUSCLES. 


MYOSITIS. 

Primary Myositis .—The few recorded cases of this disease 
have been characterized by swelling and tenderness of the 
muscles, stiffness and pain on motion, and oedema of the 
subcutaneous tissues. Atrophy of the muscles may result. 
The process may terminate fatally by involving the muscles 
of deglutition and of respiration. The spleen is enlarged, 
and an irregular erythematous eruption is usually present, 
the disease resembling an acute infection in these respects. 
Examination of the affected muscles shows marked degen¬ 
eration of the fibres, with an infiltration of the interstitial 
tissue. The course of the disease extends over several 
months or years. The diagnosis from trichinosis can be 
positively made only by microscopic examination of the 
muscle-fibres. No curative treatment is known. 

Acute purulent myositis , which is usually a complication 
of pyaemia, more rarely of other septic diseases, has occurred 
as a primary form in a few instances. 

Progressive myositis ossificans is a rare disorder in which 
the muscles undergo ossification. The process may be 
limited to certain muscles, or may be more generally dis¬ 
tributed, as in the well-known case of the “ ossified man.” 

PROGRESSIVE MUSCULAR DYSTROPHY. 

Etiology and Synonyms.—This disorder of development 
is inherited, chiefly through the mother, in three-fifths of the 

906 



PROGRESSIVE MC/SCULAR DYSTROPHY. 907 

cases, and usually appears before the tenth year, although 
its onset may be deferred until the twentieth or the twenty- 
fifth year. The disease is four times as common in boys as 
in girls. The etiology of the disease is unknown. Syno¬ 
nyms : Idiopathic muscular atrophy; Pseudo-hypertrophic 
muscular paralysis. 

Pathology.—There is an increase of connective tissue, 
and usually an increased deposit of fat about the muscular 
fibres. The muscular fibres become hypertrophied and 
their nuclei are increased in number. Degeneration of the 
fibres then ensues, and leads to atrophy, so that in advanced 
stages the muscles resemble masses of adipose tissue. A 
primary muscular atrophy may occur, with or without the 
development of dense connective tissue and of fat about the 
atrophied muscles. The spinal cord and the peripheral 
nerves are normal, the disorder being a primary disease of 
the muscles. 

Symptoms.—According to the relative proportion of 
hypertrophy or atrophy of muscular fibres, three clinical 
forms are described: 

1. Pseudo-hypertrophic muscular paralysis is the form in 
which increased connective tissue and fatty deposits are 
associated with atrophy and degeneration of the muscle- 
fibres. The first symptoms noted are a weakness of the 
muscles, usually of the calves, and an increase in their 
apparent bulk. The gait becomes awkward and clumsy, 
and there is difficulty in mounting stairs. The characteristic 
method of rising from the floor is by placing the hands on 
the knees and “ climbing up the legs.” The infraspinatus, 
the biceps, and the triceps muscles may be affected in like 
manner. The knee-jerk is normal; the reaction of degener¬ 
ation is not obtained. Later in the disease shrinkage of the 
muscle-bulk occurs, with deformities. Death, when it occurs, 
is due to some intercurrent disease. 


goS MANUAL OF THE PRACTICE OF MEDICINE. 

2. Hypertrophic paralysis is the form in which the muscles 
undergo at first a true hypertrophy, but become atrophied 
late in the disease. The symptoms are practically identical 
with those of the pseudo-hypertrophic form. 

3. The primary atrophic form differs from the preceding 
forms only in the absence of a primary enlargement of 
muscle-bulk. A number of varieties of this form are 
described, according to the distribution of the lesions. Of 
these varieties the following are the most important: 

(a) The infantile form, or the Landouzy-Dejerine type, in 
which the face and the shoulder-girdle are affected. 

( b ) The juvenile form of Erb, in which the affection first 
appears between the fifteenth and twentieth years, and in¬ 
volves the muscles of the shoulder, upper arm, gluteal 
region, and thigh. 

Prognosis.—The course of the disease extends over years ; 
the disease progresses steadily, and the outlook is bad. 

Treatment is without influence on the disease. Galvan¬ 
ism and oil-inunctions with friction may be tried. The 
general health must be improved in every way. 

PARAMYOCLONUS MULTIPLEX (MYOCLONUS 

MULTIPLEX). 

This rare disease occurs usually in adult males, and may 
be induced by fright, injury, or emotion. 

The pathology is unknown ; the disease is supposed to 
be allied to convulsive tic. 

The symptoms consist of sudden paroxysmal contrac¬ 
tions, of a clonic character, of a number of muscles; the 
patient may be thrown from a chair or from the bed by the 
violent tremors. The spasms are regularly bilateral. The 
most characteristic spasms occur in the muscles of the 
trunk and hips, but the arms, legs, and face also may be 
involved. In exceptional cases the spasms assume a tonic 


THOMSEN'S DISEASE; MYOTONIA CONGENITA. 909 

form. Between attacks there may be a general muscular 
tremor. The body-strength is usually unimpaired, although 
neurasthenic or hysterical symptoms may be present. 

Paramyoclonus is to be diagnosed from hysteria by the 
fact that the affected muscles are not physiologically 
allied, and therefore the spasmodic movements cannot be 
imitated voluntarily. 

Treatment.—Chloral and hyoscine may be employed, 
together with a tonic treatment. Hydrotherapy seems to 
do good in some instances. 

THOMSEN’S DISEASE ; MYOTONIA CONGENITA. 

This disorder, which is exceedingly rare in America, is 
practically always hereditary, and appears in childhood. 
It is unknown whether the disease is a primary disease of 
the muscles or a congenital defect in their innervation. 

The symptoms consist of painless tonic spasms, lasting 
for a few seconds, whenever voluntary motion is attempted. 
Voluntary muscular contraction and relaxation are therefore 
slow, and the muscles seem to act stiffly. The muscles 
limber up, however, after repeated use, but the spasms are 
increased by cold or nervousness. The electrical and 
mechanical excitability of the muscles is increased, and the 
muscles themselves may undergo hypertrophy, but the 
bodily strength is not always good. The disease, though 
incurable, does not tend to shorten life. 

There is no treatment for the disease, although Thomsen 
himself obtained benefit from active muscular exercise. 

Congenital paramyotonia is a primary muscular affec¬ 
tion, of a congenital and inherited character, in which 
tonic spasms are induced by exposure to cold. The spasms, 
which may occur in the extremities or in the face, may last 
from fifteen to twenty minutes. There is no known treat¬ 
ment for this disease. 









X. ANIMAL PARASITES. 


TREMATODES. 

i. Distoma hepaticmn (Fig. 71), or “ liver-fluke,” is a rare 
parasite 28 mm. long and 12 mm. broad. Its habitat is the 
small intestine, but it may enter the bile-passages and cause 

ascites and jaundice, with enlargement of 
the liver and chronic inflammation of 
the biliary passages. 

Distoma lanceolatum is a smaller 
variety infecting cattle and sheep. Dis¬ 
toma endemicum and distoma perniciosum 
are liver-flukes endemic in Japan. 

2. Bilharzia licematobia , or “ blood- 
fluke,” endemic in Egypt, Arabia, and 
Northern Africa, is the cause of the 
“endemic haematuria” of these countries. 
It is found in the abdominal veins, espe¬ 
cially the portal, splenic, renal, and mes¬ 
enteric, and is more commonly found in 
children. Haematuria, anaemia, and pain¬ 
ful and frequent micturition are the usual 

f,g. 71.— DiTtoma hepat- symptoms. The great majority of pa- 
icum (Von jaksch). tients recover, and the symptoms usually 

disappear at the time of puberty. 

3. Distoma Ringeri , or the “ bronchial fluke,” gives rise to 
cough and haemoptysis. The parasite is endemic in China 
and Japan. 

910 








OX YURIS VERMICULAR IS. 


9 II 


NEMATODES. 

Ascaris Lumbricoides. 

Ascaris lumbricoides, or round worm, resembles in ap¬ 
pearance the ordinary earth-worm. The female is from 
12 to 16 inches in length, the male about 8 inches. This 
common parasite is especially frequent in Eastern countries, 
in women and children and in the insane. The habitat of 
the worm is in the small intestine, and the number varies 
from one to many hundreds. The parasite is usually passed 
by the rectum, but in rare cases the worms may wander 
into the bile-ducts or into the stomach, from which they 
may be vomited, or may pass upward to enter the larynx, 
bronchi, nares, or even the Eustachian tube. 

The symptoms are usually mild and obscure. There 
may be vague symptoms of gastro-intestinal irritation, or 
reflex symptoms, such as itching of the nose, grinding of 
the teeth, or broken sleep. In children convulsive seizures 
due to worms are less common than is usually supposed. 

The diagnosis can be made with certainty only by the 
actual passage of a worm. 

Treatment.—Santonin may be given in doses of from y 
to i grain three times a day to a child of five years. Larger 
proportional doses may be given to adults, and the drug 
may advantageously be combined with small doses of 
calomel. Yellow vision, discolored urine, and slight delirium 
may attend the use of santonin in susceptible patients. 
When these symptoms occur the drug should at once be 
discontinued. Of equal service are the fluid extracts of 
senna and spigelia in equal parts, 3ss-j of the admixture 
being given three times a day until free purgation occurs. 

Oxyuris Vermicularis (Pin-worm; Thread-worm). 

The female worm is from io to 12 millimeters long; the 
male is one-third as long. The habitat is in the ileum and 


912 MANUAL OF THE PRACTICE OF MEDICINE . 

the large intestine; in these situations the parasite gives no 
symptoms. If the rectum be invaded, itching and burning 
of the anus, worse at night, occasion much distress. Excita¬ 
tion of the sexual organs may also result. The parasite 
may emigrate into the vagina and produce itching and 
inflammation. 

The diagnosis is made by finding the worms in the de¬ 
jections, and occasionally on the skin of the anal region. 

The treatment consists of rectal injections of lime-water, 
infusion of quassia, iced salt-water, bichloride of mercury 
(i : 10,000), or solution of alum (3j : Oj). 

Anchylostoma Duodenale. 

This worm (Strongylus duodenalis) is found in the upper 
portions of the small intestine, and is most common in 
Egypt, Italy, and Brazil. The parasite is almost unknown 
in the United States. The worm attaches itself by claw- 

a b 

f! 

Fig. 72. —Anchylostoma duodenale (Von Jaksch) : a , male, b, female, natural size ; c, male, 

enlarged. 

like teeth to the intestinal wall, and sucks blood from the 
blood-vessels. The symptoms consist of digestive disorders 
and progressive anaemia (“ Egyptian chlorosis ; ” “ St. Go- 
thard’s disease ”). 

Treatment.—Thymol should be given in 30-grain doses 
in capsule, the dose to be repeated in two hours and followed 
by a brisk purgative. 

Trichocephalus Dispar (Whip-worm). 

This parasite, which is from ^ to 2 inches long, is cha¬ 
racterized by a filiform anterior portion which occupies two- 



TRICHINA SPIRALIS. 


9 ! 3 


thirds of the entire length. The posterior portion is blunt 
and curved. Its habitat is in the caecum, where the parasite 
is frequently found in great numbers. The worm possesses 
no clinical significance. 

Trichina Spiralis. 

When raw or imperfectly cooked ham or pork containing 
muscle-trichinae is taken into the human stomach, the unde¬ 
veloped trichinae are liberated. The para¬ 
sites become perfectly developed by the 
third day, appearing as small silvery 
threads barely visible to the naked eye. 

New-born trichinae migrate into the mus¬ 
cles by the sixth day, and there assume a 
spiral form and become encysted, the cap¬ 
sule being composed of connective tissue 
which may be infiltrated by lime-salts. 

Muscle-trichinae so encapsulated may live 
for years. 

Symptoms of trichinosis appear if trichi¬ 
nae are ingested in any considerable num¬ 
ber. The symptoms appear in two stages : 

1. G astro-intestinal symptoms occur one 
or two days after the ingestion of the in¬ 
fected ham. There are nausea, vomiting, 
abdominal pain, and serous diarrhoea. In 
severe cases the symptoms mav resemble Fin 73 —Male mtesti- 

' nal trichina (a ); female 

cholera. I here may be considerable fever, intestinal trichina w.- 
In this stage very severe cases may ter- ^ s s c ^') trlchina (Von 
minate fatally. 

2. Muscular symptoms develop in from one to two weeks. 
The muscles become swollen, tender, and excessively pain¬ 
ful ; the skin over the affected muscles is usually cedematous. 
Involvement of the respiratory muscles leads to impairment 

58 



914 MANUAL OF THE PRACTICE OF MEDICINE . 

of respiratory power, dyspnoea, and liability to bronchitis 
and broncho-pneumonia. CEdema of the eyelids usually 
appears by the seventh day, and is the most characteristic of 
the early symptoms. Fever of an irregular type is usually 
present, and profuse sweating is commonly observed. Al¬ 
buminuria occurs in the majority of cases. The knee- 
reflexes are usually lost. 

The diagnosis is aided by the fact that a number of indi¬ 
viduals are usually affected at the same time. In doubtful 
cases a small piece of muscle may be excised under cocaine- 
anaesthesia and examined. 

The duration of the acute symptoms is from two to eight 
weeks. Recovery is slow and tedious. 

The prognosis is grave, 30 per cent, of the cases termi¬ 
nating fatally, chiefly by pulmonary complications. 

Treatment.—Prophylactic treatment consists in the gov¬ 
ernmental inspection of ham and pork and the thorough 
cooking of the meat. 

During the gastro-intestinal stage brisk purgatives should 
be administered. The use of glycerin in 3ss doses every 
hour has been recommended. Thymol in 3j doses in cap¬ 
sule is also of service. When migration into the muscle has 
occurred the treatment can only be palliative. 

Filaria Sanguinis Hominis. 

The adult worm is from 4 to 5 inches long, and in the 
human subject probably lodges in some large lymphatic 
vessel. The female produces an enormous number of em¬ 
bryos from y^-g- to of an inch long and of the width of a 
red blood-cell. The embryos enter the blood-current, and 
are present in the blood during the night, but disappear 
during the day-time. Should the patient sleep during the 
day and work at night, the migrations of the parasites 
become diurnal. It is supposed that infection occurs 



CESTODES. 915 

through the agency of mosquitoes. The parasite is most 
common in tropical and sub-tropical countries. 

Symptoms are caused by the blocking of the lymph- 
channels by the adult worm or 
the ova. Haematochyluria (or 
chyluria) is the most common 
symptom. The passage of chy¬ 
lous urine with or without the 
admixture of blood is inter¬ 
mittent and is not inconsistent 

with good general health. Fig ' 74 '~ F ( ‘y ™jTksxh” h ° mmis 

Among the other symptoms 

may be mentioned lymph-scrotum, chylous hydrocele, 
chylous ascites, and elephantiasis. 

The diagnosis of parasitic chyluria from the non-para- 
sitic form is made by the finding of the embryos in the blood 
drawn about midnight. 

The prognosis is generally favorable. 

Treatment.—Gallic acid (<5j-ij doses daily) and large 
doses of potassium iodide have been of service. The treat¬ 
ment by methyl-blue has apparently been followed by good 
results. 



CESTODES (T-ffiNLffi; TAPE-WORMS). 

When the eggs of the taenia enter the stomach of animals 
the embryos become liberated; they then migrate to other 
organs, where they form encysted larvae or scolices, known 
as “ cysticerci.” A cysticercus is therefore an undeveloped 
tape-worm. Meat containing cysticerci is said to be 
“ measly,” and if eaten raw or imperfectly cooked the cysti¬ 
cerci develop into mature form within the alimentary canal 
of their host. Three chief varieties of tape-worm are encoun¬ 
tered in the human subject. 

1. Tcenia solium is from 6 to 8 feet long. The head, which 



91 6 MANUAL OF THE PRACTICE OF MEDICINE. 

is the size of the head of a pin, is marked by four suckers 

and a double row of hooklets. 
The neck is about an inch long. 
The joints or proglottides, 
which contain male and female 
organs of generation, become 
larger and more mature the 
further they are from the head. 
Taenia solium is usually single, 
and develops in man from eat¬ 
ing measly pork or ham. 

2. Tcenia saginata or medio - 
canellata , which is the most 
common form in the United 
States, develops from eating 
measly beef. The worm is 
longer than the taenia solium, 
and the sexual apparatus of the 
mature segments is somewhat 
different. The head possesses 
four suckers, but no hooklets. 

3. Bothriocephalli s latus, which 
is common in the German 
Baltic provinces and rare in the 
United States, develops from 
eating infected fish. The head 
is club-shaped, with two slit¬ 
like suckers on the side. The 
segments are short but broad, 
and the parasite frequently 
grows to a length of from 25 
to 30 feet. 

Symptoms are indefinite. 
There may be digestive disturbances, abdominal pain, diar- 



Fig. 75. —Small portions from different 
parts in the length of a tape-worm; 
natural size (Griffith). 





ECHINOCOCCUS DISEASE. 


9i; 


rhcea, and inordinate appetite. The patient may lose flesh 
and strength. Ihere may be reflex phenomena—itching 
of the nose, salivation, nervous vomiting, and great mental 
depression. The diagnosis can be made with certainty only 
by finding the links in the dejecta. 

The growth of the bothriocephalus latus is frequently 
accompanied by progressive anaemia. 

Treatment is successful only when the head of the worm 
is passed. In all cases the patient should be ordered a very 
light diet for two days; a saline purgative should be given 
on the second night, and the next morning the taeniafuge 
should be given on a fasting stomach and followed in two 
hours by a brisk purge. 

Among the efficient anthelminthics recommended are 
fluid extract of male fern (sij dose), infusion of pome¬ 
granate (2 to 3 ounces of the bark in Oj of water), infusion 
of pumpkin-seeds, and koosso (sss of the dried flowers in 
water). Tanret’s tannate of pelletierine may be given in a 5- 
to 10-grain dose, but the remedy is very expensive. Good 
results have followed 3ss doses of oil of pine-needles given 
in emulsion or in capsule. 

ECHINOCOCCUS DISEASE. 

(See Hydatids of the Liver) 

For the rarer forms of animal parasites the reader is re¬ 
ferred to larger works. 
































































INDEX. 


Abscess, perinephritic, 666 

subphrenic. See Perihepatitis, acute. 
Acetonuria, 625 
Acromegaly, 904 
Actinomyces, 179 

Actinomycosis, etiology and pathology, 
179 

prognosis, 180 

symptoms and treatment, 180 
Addison’s disease, 731 
pathology, 731 
symptoms, 732 
treatment, 733 
Albuminuria, 614 
tests for, 616 

Amyloid degeneration, intestinal ulcers 
due to, 518 
Anaemia, 712 
pernicious, 718 
pathology, 718 
symptoms, 720 
treatment, 721 
secondary, 712 

pathology and symptomatology, 
713 

treatment 715 
Aneurysm, 281 

of abdominal aorta, 290, 291 
of thoracic aorta, 283 
diagnosis, 287 
physical signs, 286 
prognosis, 288 
treatment, 289 
Angina pectoris, 266 

prognosis and treatment, 268 
symptoms, 267 
pseudo-, 269 
Animal parasites, 910 
Ankylostoma duodenale, 912 
Anthrax, 163 

definition and synonyms, 163 


Anthrax, etiology, 163 
symptoms, 163 
treatment, 165 

of the disease, 168 
preventive inoculations, 167 
Aortic regurgitation, 234 
stenosis, 239 
Apoplexy, 749 
pulmonary, 323 
Appendicitis, 505 
acute catarrhal, 506 

course of the disease, 508 
pathology and symptoms, 506 
physical examination, 507 
symptoms, 506 
acute suppurative, 508 

course of the disease, 511 
pathology, 508 
physical signs, 510 
symptoms, 509 
chronic, 515 
gangrenous, 513 
prognosis, 513 
treatment, 514 
ulcerative, 508 

Arteries, cerebral, aneurysm of, 758 
embolism of, 755 

etiology and pathology, 755 
diagnosis, 757 
symptoms, 756 
treatment, 757 

hemorrhage and embolism of, dif¬ 
ferential diagnosis, 757 
thrombosis of, 758 
diseases of, 277 
Arterio-sclerosis, 277 
pathology, 278 
physical signs, 280 
symptoms, 279 
treatment, 280 
Arteritis, syphilitic, 281 


919 








INDEX. 


920 

Arthritis deformans, 686 

pathology and symptoms, 687 
prognosis and treatment, 689 
rheumatoid. See Arthritis defor¬ 
mans. 

Ascarides lumbricoides, 901 
Ascites, 553 
tubercular, 549 
Asphyxia, local, 900 
Asthma, 313 

causes, exciting, 314 
predisposing, 313 
definition and etiology, 313 
pathology and symptoms, 314 
physical signs, 315 
prognosis and treatment, 316 
thymic, 292 
Asthma-crystals, 316 
Ataxia, hereditary, 821 
locomotor, 813 

Charcot’s knee in, 818 
Atheroma, 225. See Arteriosclerosis. 
Atrophy, acute yellow. See Hepatitis , 
parenchymatous, acute. 
cerebral, in children, 778 

etiology and symptoms, 778 
treatment, 780 

facial, progressive unilateral. See 
Hemiatrophy, facial. 
progressive muscular, 804 
diagnosis, 806 
pathology, 804 
prognosis, 807 
symptoms, 805 
treatment, 807 

Auditory nerve, diseases of, 838 

Bacillus, comma, 127 

Klebs-Loeffler. See Plate 10. 
leprae, 173 
tetani, 169 
typhosus, 18 

Basedow’s disease. See Exophthalmic 
goitre. 

Bell’s mania. See Delirium, acute. 

palsy, 835 
Beri-beri, 854 
Bilharzia haematobia, 910 
Blood, diseases of, 712 

vomiting of, in ulcer of the stomach, 
461 

Blood-fluke, 910 
Bothriocephalus latus, 916 


Bowels, changes in, in cancer of the 
intestine, 523 

hemorrhages from, in typhoid fever, 
28 

Brachycardia, 264 
Bradycardia, 264 
Brain, abscess of, 769 

pathology and symptoms, 770 
treatment, 771 

blood-vessels of, anaemia of, 748 
congestion of, 747 
oedema of, 749 
cortical areas of, 764 
gummata of, 786 
membranes of, diseases of, 736 
subcortical areas of, 768 
syphilis of, 785 
symptoms, 787 
treatment, 788 
tumors of, 772 

pathology and symptoms, 773 
treatment, 777 

Brain-substance, diseases of, 764 
Brand, method of, in treatment of 
typhoid fever, 42 

Breast-pang. See Angina pectoris. 
Bright’s disease, acute. See A T ephritis. 
chronic, 635 

Bright’s hypertrophy of the heart, high 
tension in, 205 
Brodie’s joint, 893 
Bronchi, diseases of, 302 
Bronchial fluke, 910 
Bronchiectasis, 310 
Bronchitis, capillary. See Broncho¬ 
pneumonia. 
catarrhal, acute, 302 
chronic, 308 
croupous, acute, 306 
chronic, 310 

diphtheritic. See Bronchitis, acute 
croupous. 

membranous, fibrinous, and plastic. 
See Bronchitis, chronic 
croupous. 

Broncho-pneumonia, 341 
cerebral cases, 346 
course and termination, 346 
in adults, 348 

prognosis and treatment, 350 
pathology, 342 
physical signs, 346 
symptoms, 344 





INDEX. 


921 


Cachexia, malarial, 160 
treatment, 162 
strumipriva, 903 
Caisson-disease, 796 
Calculi, biliary. See Cholelithiasis. 
renal, 659 

Calomel fumigation in treatment of 
diphtheria, 114 
Caput coli, cancer of, 524 
Cardiac affections complicating rheu¬ 
matism, 670 
Cardialgia, 447 

Cerebral complications of rheumatism, 
671 

Cestodes, 915 
Charbon. See Anthrax. 
Charcot-Leyden’s asthma-crystals, 316 
Charcot’s joint in locomotor ataxia, 818 
Chicken-pox. See Varicella. 
Chloro-anoemia. See Chlorosis. 
Chloroform inhalations in treatment of 
hydrophobia, 168 
Chlorosis, 716 

Cholecystitis, suppurative, 599 
Cholelithiasis, 594 
symptoms, 596 
treatment, 601 
Cholera, 126 
bacillus of, 127 

complications and sequela;, 131 
contagiousness of, 128 
definition and synonym, 126 
etiology, 127 
incubation period, 128 
infantum, 492 

in meat-fed children, 495 
morbus, 496 
pathology, 128 
prognosis, 131 
stage of collapse, 130 
stage of preliminary diarrhoea, 129 
stage of purging, 129 
stage of reaction, 130 
symptoms, 128 
treatment, medicinal, 132 
prophylactic, 131 
warm or tepid stage, 130 
Cholerine, 131 
Chorea, 873 
habit-, 879 
Huntingdon’s, 879 
insaniens, 874 
symptoms, 874 


Chorea, treatment, 877 
Chyluria, 624 

Circulatory system, diseases of, 183 
Cirrhosis, biliary, 570 
^ fatty, 571 
Coccygodynia, 858 
Colic, biliary, pulse in, 597 
mucous. See Colitis, mucous. 
Colitis, mucous, 487 
Compression-myelitis, 829 
Congestions, venous, acute, in dilata¬ 
tion of the heart, 208 
chronic, in dilatation of the heart, 
209 

Constitutional diseases, 667 
Consumption, chronic. See Phthisis, 
chronic pulmonary. 
galloping. See Phthisis, acute ptil- 
monary. 

Convulsions, infantile, 860 
causes, 860 
Cor adiposum, 254 
Coup de soleil, 896 
Cramp, writer’s, 884 
Cranial bones, syphilis of, 786 
nerves, diseases of, 831 
Creosote in treatment of tuberculosis, 
398 

Cretinism, 902 
Croup, spasmodic, 293 
Curschmann’s spirals, 315 
Cyst, echinococcus, 583 
Cysts, pancreatic, 609 

Degeneration, amyloid, following 
tertiary syphilis, 142 
reaction of, 800 
Delirium, acute, 871 
tremens, 898 

Dementia, paretic. See Paresis, gen¬ 
eral. 

Dengue, 94 

convalescence from, 95 
etiology, 94 

pathology and symptoms, 94 
prognosis and treatment, 95 
Diabetes insipidus, 697 
treatment, 698 
mellitus, 689 
diet in, 695 

etiology and pathology, 690 
symptoms, 691 
treatment, 695 





922 INDEX. 


Diarrhoea, acute dyspeptic, in children, 
49 ° 

chronic. See Enteritis , chronic 
catarrhal. 

in intestinal ulceration, 520 
morning, 480 
summer, in children, 490 
Diarrhoeal diseases of children, 489 
cholera infantum, 492 
diarrhoea, acute dyspeptic, 490 
entero-colitis, acute, 490 
Digestive system, diseases of, 432 
Diphtheria, 102 
antitoxine of, 115 
complicating lesions, 105 
complications and sequelae, 109 
definition, 102 
essential lesion, 104 
etiology, 102 
immunity from, 103 
incubation period, 105 
laryngeal, 108 
local, 105 

method of infection, 103 
mortality, 111 
nasal, 108 
pathology, 104 
pharyngeal, 107 
prognosis, 111 
serum-therapy, 115 
symptoms, 105 
tonsillar, 106 
treatment, ill 
general, 112 
local, 112 
prophylactic, 111 

Diplococcus pneumoniae of Frankel, 
325 

Diseases, constitutional, 667 
Distoma hepaticum, 910 
lanceolatum, 910 
Ringeri, 910 
Dropsy, abdominal, 553 
Duchenne’s paralysis, 803 
Duodenum, cancer of, 525 
round ulcer of, 516 
ulceration of, after burns, 517 
Dura mater, cerebral, diseases of, 736 
haematomaof. Szz Pachymen¬ 
ingitis, chronic internal. 
spinal, diseases of, 788 
Dysentery, 497 

acute, treatment, 503 


Dysentery, acute, treatment: amoebic 
form, 504 
catarrhal form, 503 
croupous form, 504 
catarrhal, acute, 498 
treatment, 503 
chronic, 504, 505 
croupous, acute, 501 
treatment, 504 
tropical or amoebic, 499 
treatment, 504 

Dyspepsia, chronic. See Gastritis , 
chronic catarrhal. 
nervous, 475 

Dystrophy, progressive muscular, 906 

Echinococcus, 583 

cyst. See Liver , hydatid of. 
cysts of the lung, 368 
disease, 917 

Eclampsia, infantile, 860 

Effusion in pleurisy, mechanical effects 
of, 404 

Emphysema, interlobular, 355 
vesicular, 356 
pathology, 357 
physical signs, 360 
prognosis, 360 
symptoms, 358 
treatment, 361 
variations, 359 

Empyema, 411 

Encephalitis, suppurative, 769 

Endarteritis, cerebral, 761 
illustrative case, 762 
pathology and symptoms, 761 
prognosis and treatment, 763 
chronic. See Arteriosclerosis. 
syphilitic, 786 

Endocarditis, acute, 212 

course of the disease, 217 
effects of the lesion, 215 
etiology, 213 
pathology, 214 
physical signs, 216 
prognosis, 217 
symptoms, 215 
treatment, 218 
chronic, 223 
treatment, 243 

complicating lobar pneumonia, 337 
malignant, 219 
diagnosis, 222 





INDEX. 


923 


Endocarditis, malignant, duration, 222 
etiology, 219 
lesion, 219 
prognosis, 223 
symptoms, 220 
treatment, 223 

Enteritis, catarrhal, acute, 481 
etiology, 481 

pathology and symptoms, 482 
prognosis and treatment, 483 
catarrhal, chronic, 483 
etiology, 483 

pathology and symptoms, 484 
prognosis and treatment, 485 
phlegmonous, 486 
pseudo-membranous, 486 
Entero-colitis, acute, in children, 490 
Enterorrhagia, 531 
Epilepsy, 862 

and hystero-epilepsy, differential 
diagnosis, 867 
causes, 862 
diagnosis, 866 
Jacksonian, 866 
nocturnal, 865 
pathology, 863 
procursive, 863 
prognosis and treatment, 867 
symptoms, 863 

Epithelioma of the stomach, 465 
Erysipelas, 117 
complications, 120 
definition, 117 
etiology, 117 
metastatic, 119 
migrans, 119 
pathology, 117 
prognosis, 120 

streptococci of, effect on tumor-cells, 
120 

symptoms, general, 118 
local, 118 

traumatic and idiopathic forms, 117 
treatment, general, 120 
local, 121 
prophylactic, 120 

Eshbach’s test for albumin in urine, 
617 

Expiration, forced, arrangement of bot¬ 
tles for, 415 

Facial nerve, spasm of, 838 
Farcy. See Glanders. 


Fecal accumulation, 533 
Fever, breakbone. See Dengue. 
cerebro-spinal. See Meningitis , epi¬ 
demic cerebro-spinal. 
fermentation-, 124 
in abscess of the liver, 575 
malarial. See Malarial fever. 
relapsing. See Relapsing fever. 
rheumatic, 667 
scarlet. See Scarlet fever. 
thermic, 896 
treatment, 897 

typhoid. See Typhoid fever. 
yellow. .See Yellozvfever. 
Fibro-serous membranes, inflammation 
of, in acute articular rheuma¬ 
tism, 669 

Fifth nerve, diseases of, 833 
Filaria sanguinis hominis, 914 
Foot-drop, 851 

Foramen ovale, patency of, congenital, 
275 

Fourth nerve, diseases of, 833 
Friedreich’s ataxia. See Ataxia , hered¬ 
itary. 

Gall-bladder, calculi in, 594 
Gall-ducts, cancer of, 602 
Gall-stones. See Cholelithiasis. 
Gangrene, local or symmetrical, 900 
Garland’s S-curve, 406 
Gastralgia, 477 
Gastrectasis, 452 

Gastric juice, hyperacidity of, 476 
hypersecretion of, 476 
Gastritis, catarrhal, acute, 440 

etiology and synonyms, 440 
from ptomaine-poisoning, 441 
pathology and symptoms, 440 
treatment, 441 
chronic, 445 

etiology and pathology, 445 
prognosis, 449 
treatment, 449 

dietetic and hygienic, 449 
medicinal, 450 
croupous, acute, 443 
diphtheritic. See Gastritis , acute 
croupous. 

gastric, acute. See Gastritis , acute 
catarrhal. 

membranous. See Gastritis, acute 
croupous. 









924 


INDEX. 


Gastritis, mycotic and parasitic, 444 
phlegmonous. See Gastritis , acute 
suppurative. 

purulent. See Gastritis, acute sup¬ 
purative. 
sclerotic, 446, 449 
simple, 446, 449 
suppurative, acute, 444 
toxic, 442 

symptoms and treatment, 443 
Gastro-duodenitis. See Jaundice, 
catarrhal. 

Gastrodynia, 477 

Gastrorrhagia. See Stomach, hemor¬ 
rhage from. 

Glanders, 176 
acute, 177 
chronic, 178 

definition and synonym, 176 
etiology, 176 
lesion, 177 
symptoms, 177 
treatment, 178 

Glosso-pharyngeal nerve, diseases 
of, 840 

Glottis, oedema of. See Laryngitis, 
oedematous. 

Glycosuria, 625, 696 
Goitre, exophthalmic, 271 
prognosis, 273 
treatment, 274 
Gout, 678 

associated lesions of, 680 
etiology, 678 
pathology, 680 

rheumatic. See Arthritis defor¬ 
mans. 

symptoms, 681 
treatment, 684 
Grand mal, 863 
aurae in, 863 

Graves’ disease. See Exophthalmic 
goitre. 

Green sickness. See Chlorosis. 

“ Griffin-claw,” 805 
Gummata in the lung, 365 
in the myocardium, 253 
of syphilis, 141 
of the brain, 786 

H/f.matf.mf.sis. See Stomach, hemor¬ 
rhage from. 

Hcematoma, mediastinal, 431 


Hematuria, 617 
Haemoglobinuria, 619 
paroxysmal, 620 
toxic, 619 

Haemopericardium, 197 
Haemophilia, 709 
symptoms, 710 
treatment, 711 
Haemoptysis, 320 

and haematuria, difilerential diagnosis, 
474 

arthritic, 321 
Haemothorax, 426 
Headache, sick. See Migraine. 

Heart, aneurysm of, 259 

symptoms, prognosis, and treat¬ 
ment, 260 
dilatation of, 206 
physical signs, 211 
symptoms, 207 
diseases of, 198 
fatty, 254 

hypertrophy of, 202 
symptoms, 203 
intermittent action of, 263 
malformations of, congenital, 275 
symptoms and treatment, 277 
neuralgia of. See Angina pectoris. 
neuroses of, 261 
palpitation of, 261, 262 
rupture of, 260 

symptoms, prognosis, and treat¬ 
ment, 261 
Heartburn, 447 

Heart-muscle, poisoning of, 255 
weakness of, 198 
Heat-exhaustion, 895 
Heat-stroke, 896 
Heberden’s nodes, 687 
Heller’s test for albumin in urine, 616 
for blood in urine, 618 
Hemiatrophy, facial, 901 
Hemicrania. See Migraine. 
Hemiplegia, infantile, 778 
Hemorrhage between cerebral dura 
mater and pia mater, 746 
between cerebral dura mater and the 
bones of the skull, 745 
broncho-pulmonary, 320 
cerebral, 749 
etiology, 749 
pathology, 750 
prognosis, 754 






INDEX . 925 


Hemorrhage, cerebral, symptoms, 751 
treatment, 754 

from the bowels in typhoid fever, 29 

in cancer of the intestine, 523 

in intestinal ulceration, 520 

in jaundice, 591 

into the spinal cord, 795 

into the spinal membranes, 793 

meningeal, 745 

pulmonary, 320 

renal, 617 

Hemorrhages in cancer of the stomach, 
468 

in chronic pulmonary phthisis, 390 
Hemorrhagic infarct, 323 
Henoch’s disease, 708 
Hepatitis, interstitial, chronic. See 
Liver , cirrhosis of. 
parenchymatous, acute, 562 
suppurative, 573 

Hodgkin’s disease. See Pseudo-leu- 
kccmia. 

Huntingdon’s chorea, 879 
Hutchinson’s teeth, 147 
Hydrocephalus, chronic, 784 
acquired, 785 
congenital, 784 
treatment, 785 
Hydronephrosis, 657 
Hydropericardium, 196 
Hydroperitoneum, 553 
Hydrophobia, 165 
etiology, 165 
incubation period, 166 
pathology, 166 
prognosis, 167 
symptoms, 166 
treatment, 167 
Hydro-pneumothorax, 420 
Hydrothorax, 425 

Hyperacidity of gastric secretions, 476 
Hyperpyrexia in rheumatism, 671 
Hypersecretion of gastric juice, 476 
Hypoglossal nerve, diseases of, 846 
Hysteria, 887 
symptoms, 888 
circulatory, 892 
digestive, 891 
joint, 893 
mental, 893 
motor, 888 
respiratory, 892 
sensory, 890 


Hysteria, symptoms: special senses, 891 
temperature, 893 
urinary, 892 
treatment, 894 

Icterus. See Jaundice. 

Impaction, fecal, complete, 534 
incomplete, 535 
Incompetency, mitral, 226 
Indicanuria, 624 
Indigestion, acute, 441 
Infection, septic, 124 
Infectious diseases, 17 
Influenza, epidemic, 89 
bacillus of, 89 

complications and sequelae, 91 
pneumonia, 91 
convalescence from, 92 
treatment during, 93 
course, 91 

definition and synonym, 89 
duration, 92 
etiology, 89 
lesions, 89 

complicating, 89 
prognosis, 92 
symptoms, 90 
catarrhal, 90 
gastro-intestinal, 91 
nervous, 90 
of infection, 90 
treatment, 92 

Inoculations, preventive, in treatment 
of hydrophobia, 167 
Insolation, 896 

Intestinal obstruction from foreign 
bodies, 527 

from strictures and tumors, 527 
Intestine, amyloid degeneration of, 536 
cancer of, 521 
pathology, 522 
hemorrhage from, 531 

symptoms and treatment, 532 
non-cancerous tumors of, 525 
ulceration of, 5^ 
symptoms, 520 
treatment, 521 
varieties, 

Intestines, diseases of, 480 
Intoxication, septic, 124 

Jaundice, 589 
bowels in, 591 



926 


INDEX. 


Jaundice, catarrhal, 592 

febrile, acute. See Weils disease. 
malignant. See Hepatitis, paren¬ 
chymatous , acute. 
temperature in, 592 
urine in, 591 

Kak-KE, 854 
Kidney, amyloid, 647 
congenital cystic, 656 
cysts of, 655 

fatty. See Kidneys, chronic degen¬ 
eration of. 

floating. See Kidney, movable. 
movable, 612 

palpable. See Kidney , movable. 
suppurative disease of, 650 
etiology, 650 

pathology and symptoms, 651 
treatment, 653 
surgical, 650 

tubercular diseases of, 648 
tuberculosis of, 648 
tumors of, 653 
symptoms, 654 
treatment, 655 
waxy degeneration of, 647 
Kidneys, congestion of, acute, 625 
chronic, 626 

degeneration of, acute, 627 
chronic, 628 
diseases of, 612 

malformations of, congenital, 612 
Knee-jerk, loss of, in locomotor ataxia, 

81 5 

Koch, bacillus of, 127 
Koch’s lymph in treatment of tuber¬ 
culosis, 398 

La grippe. See Influenza, epidemic. 
Landry’s paralysis. See Paralysis, 
acute ascending. 

Laryngismus stridulus, 292 
Laryngitis, catarrhal, acute, 294 
chronic, 296 
membranous, 297 
oedematous, 301 
spasmodic, 293 
syphilitic, 300 
tubercular, 298 
Larynx, diseases of, 292 
spasm of, 292 
Lead-paralysis, 853 


Leontiasis, 174 
Leprosy, 173 
anaesthetic, 174 
bacillus of, 173 
definition, 173 
etiology, 173 
pathology, 173 
prognosis, 176 
symptoms, 174 
treatment, 176 
tubercular, 174 
Leptomeningitis, acute, 790 
chronic, 792 
Leucocythaemia, 722 
Leucocytosis, 722 
Leukaemia, 722 
blood-changes in, 723 
diagnosis and prognosis, 726 
etiology and pathology, 722 
lymphatic, 724 
pseudo-, 727 
spleen in, 724 
symptoms, 725 
treatment, 726 
Lipuria, 625 
Lithaemia, 622 
Liver, abscess of, 573 
course, 577 
diagnosis, 578 
pathology, 574 
physical examination, 576 
symptoms, 575 
treatment, 579 
amyloid, 588 

blood-vessels of, diseases of, 603 
capsule of, diseases of, 560 
circulatory disturbances of, 559 
cirrhosis of, 565 
atrophic, 565 
fibrous, 565 
hypertrophic, 570 
syphilitic, 571 
congestion of, passive, 559 
diseases of, 556 
tubercular, 579 
fatty, 586 

functional disturbances of, 556 
gummata of, 572 
hydatid of, 583 

lardaceous. See Liver, amyloid. 
new growths of, 579 
“ nutmeg,” 559 
size of, in cirrhosis, 598 




INDEX. 


927 


Liver, waxy. See Liver , amyloid. 
Liver-fluke, 910 
Localization, cerebral, 764 
Lock-jaw, 834. See Tetanus. 
Locomotor ataxia, 813 

diagnosis, differential, 819 
localization of lesion in, 814 
pain in, 815 
pathology, 813 
perverted sensations in, 815 
prognosis, 819 
symptoms, 815 
treatment, 820 
trophic changes in, 818 
visceral crises in, 817 
Lung, abscess of, 364 
echinococcus cysts of, 368 
gangrene of, 362 
symptoms, 363 
treatment, 364 
gummata in, 365 
new growths of, 366 
syphilis of, 365 

tubercular inflammations of, 369 
conditions favorable to infection, 
370 

modes of infection, 369 
secondary inflammatory pro¬ 
cesses, 373 

structure of tubercle, 371 
symptoms, 373 
white hepatization of, 365 
Lungs, circulatory disturbances of, 318 
congestion of, 318 
diseases of, 318 
oedema of, 319 
Lymphadenitis, 427 
Lymph-glands, tuberculosis of, 733 
pathology and symptoms, 734 
treatment, 735 

Malarial fever, 152 
clinical forms, 155 

intermittent fever, 155 
malarial cachexia, 160 
pernicious intermittent fever, 
157 

pernicious remittent fever, 159 
remittent fever, 158 
conditions favoring infection, 153 
definition, 152 
diagnosis, 160 
etiology, 152 


Malarial fever, pathology, 154 
prognosis, 160 
treatment, 161 
quinine in, 161 
Mania a potu, 898 
Measles, 76 

complications and sequelae, 79 

contagion of, 77 

definition and synonyms, 76 

German. See Rubella. 

pathology, 77 

prognosis, 80 

symptoms, 77 

stage of eruption, 78 
stage of invasion, 77 
treatment, 80 
variations in course of, 79 
Mediastinum, abscess of, 430 
diseases of, 427 
emphysema of, 430 
tumors of, 428 
Melaena neonatorum, 473 
Meniere’s disease, 839 
Meningitis, chronic, 744 
complicating lobar pneumonia, 337 
epidemic cerebro-spinal, 95 
anomalous cases, 99 
complications, 100 
definition and synonym, 95 
etiology, 95 
pathology, 96 
prognosis, 101 
sequelae, 100 
symptoms, 97 
treatment, 101 
non-tubercular, acute, 741 
etiology, 741 
pathology, 742 
symptoms, 743 
treatment, 744 
syphilitic, 744, 786 
tubercular, 739 

and simple, differential diagnosis, 

743 

Merycismus, 480 
Migraine, 882 
Milk sickness, 181 
Milzbrand. See Anthrax. 

Mitral incompetency, 226 
stenosis, 230 
Morbus maculosus, 706 
Morphine hypodermically in treatment 
of hydrophobia, 168 





928 


INDEX. 


Mumps. See Parotitis, epidemic. 
Muscles, diseases of, 906 
laryngeal, spasm of, 842 
Mycosis intestinalis, 164 
Myelitis, acute and chronic, 822 
pathology, 822 
prognosis, 826 
symptoms, 823 
treatment, 826 
compression-, 829 
Myocarditis, acute, 249, 250 
chronic, 251, 252 
diffuse fibroid, 252 
syphilitic, 252 

Myocardium, degeneration of, 253 
pathology and symptoms, 256 
physical signs, 258 
prognosis and treatment, 258 
diseases of, 249 
gummata in, 253 
Myoclonus multiplex, 908 
Myositis, 906 

ossificans, progressive, 906 
Myotonia congenita, 909 
Myxoedema, 902 
operative, 903 
treatment, 903 

Necrosis, anaemic, of myocardium, 
253 

Nematodes, 911 
Nephritis, chronic, 635 
diffuse, acute, 632 

chronic, with exudation, 635 
course, 638 

etiology and synonyms, 635 
pathology, 636 
prognosis, 639 
symptoms, 637 
treatment, 639 
without exudation, 639 
cause, 644 

etiology and synonyms, 639 
lesions, complicating, 641 
pathology, 640 
prognosis, 645 
symptoms, 641 
treatment, 645 
exudative, acute, 629 
parenchymatous. See Kidneys, de¬ 
generation of, acute. 
Nephrolithiasis, 659 
etiology, 659 


Nephrolithiasis, pathology, 660 
symptoms, 660 
treatment, 664 

Nephroptosis. See Kidney, movable. 
Nerve, auditory, diseases of, 838 
facial, diseases of, 835 
spasm of, 838 
fifth, diseases of, 833 
neuralgia of, 834 
fourth, diseases of, 833 
glosso-pharyngeal, diseases of, 840 
hypoglossal, diseases of, 846 
olfactory, diseases of, 831 
optic, diseases of, 831 
pneumogastric, diseases of, 840 
seventh, diseases of, 835 
sixth, diseases of, 834 
spinal accessory, diseases of, 844 
third, diseases of, 832 
Nerve-fibres, degeneration of, 849 
normal, 849 

Nerve-trunks, tumors of, 855 
Nerves, cranial, diseases of, 831 
peripheral, diseases of, 847 
Nervous diseases, general, 860 
system, diseases of, 736 
Neuralgia, 856 

cervico-brachial, 857 
cervico-occipital, 857 
clinical varieties, 857 
intercostal, 858 
lumbar, 858 

prognosis and treatment, 859 
symptoms, 856 
trifacial, 857 
Neurasthenia, 885 
treatment, 887 
Neuritis, alcoholic, 851 
coal-gas, 854 
localized, 847 
interstitial, 848 
parenchymatous, 848 
prognosis and treatment, 850 
multiple, 850 
symptoms, 850 
treatment, 854 
optic, in brain-tumors, 774 
post-febrile, 852 
symptoms, 849 
Neuroma, plexiform, 855 
Neuromata, 855 
Neuroses, occupation-, 884 
Nodules, rheumatic, 672 




INDEX. 


929 


Obstruction, intestinal, 525 
diagnosis, 528 
etiology and pathology, 525 
prognosis and treatment, 530 
symptoms, 528 
Occupation-neuroses, 884 
(Edema, acute circumscribed, 900 
angio-neurotic, 900 
malignant. See Anthrax. 
(Esophagismus, 437 
(Esophagitis, acute, 432 
chronic, 433 

(Esophagus, dilatations and diverticula 
of, 438 

diseases of, 432 
paralysis of, 439 
rupture of, 439 
stenosis of, 433 
spasmodic, 437 
stricture of, 433 
cancerous, 435 
cicatricial, 435 
varix of, 439 

Olfactory nerve, diseases of, 831 
Ophthalmoplegia externa, 810 
interna, 810 

Optic nerve, diseases of, 831 
neuritis in brain-tumors, 774 
Osteoarthropathy, hypertrophic pulmo¬ 
nary, 905 
Oxaluria, 624 
Oxyuris vermicularis, 911 

Pachymeningitis, external, acute, 

736 

internal, acute, 736 
chronic, 737 
syphilitic, 738 
Palsy, Bell’s, 835 

shaking. See Paralysis agitans. 
wasting. See Atrophy , progressive 
muscular. 

Pancreas, cancer of, 610 
diseases of, 605 
hemorrhage into, 605 
Pancreatic cysts, 609 
Pancreatitis, chronic, 608 
gangrenous, 607 
hemorrhagic, acute, 606 
suppurative, 608 
Paralysis, acute ascending, 827 
agitans, 869 
arsenical, 853 

59 


Paralysis, atrophic spinal, 797 
Brown-Sequard’s, 830 
bulbar, 808 
acute, 808 
chronic, 808 
diver’s, 796 
facial, 835, 837 

glosso-labio-laryngeal. See Paraly¬ 
sis, bulbar. 

infantile. See Poliomyelitis , ante¬ 
rior, in children. 

Landry’s. See Paralysis , acute as¬ 
cending. 
laryngeal, 841 
lead-, 853 

muscular, hypertrophic, 908 
primary atrophic, 908 
pseudo-hypertrophic, 907 
syphilitic, 787 

Paramyoclonus multiplex, 908 
Paramyotonia, congenital, 909 
Paraplegia, ataxic, 821 
spastic, of infants, 812 
Parasites, animal, 910 
Paresis, general, 782 
Parkinson’s disease. See Paralysis 
agitans. 

Parotitis, epidemic, 83 

complications and sequelae, 84 
definition and synonym, 83 
etiology, 83 
lesion, 83 
symptoms, 83 
treatment, 84 
Peliosis rheumatica, 705 
Peptonuria, 621 
Pericarditis, 183 

and dilatation, differential diagnosis, 
190 

cancerous, 196 

chronic adhesive, 193 

clinical types, 189 

complicating lobar pneumonia, 337 

diagnosis, 190 

etiology, 183 

lesion, 184 

physical signs, 187 

prognosis, 191 

purulent, 192, 193 

pathology and symptoms, 192 
prognosis and treatment, 193 
symptoms, 186 
terminations, 185 




930 


INDEX. 


Pericarditis, treatment, 191 
tubercular, 195, 196 
Pericardium, diseases of, 183 
Periencephalitis, acute. See Delirium, 
acute. 

Perihepatitis, acute, 560 
chronic fibrinous, 561 
syphilitic, 572 
Perinephritic abscess, 666 
Peristaltic unrest, 479 
Peritoneum, cancer of, 551 
diseases of, 536 

tubercular inflammations of, 547 
tuberculosis of, acute, 547 
Peritonitis, acute, 536 
bacteriology, 537 
etiology, 536 
varieties, 537 
chronic, 545 

circumscribed, acute, 542 
treatment, 544 
diffuse, acute, 538 
diagnosis, 541 
pathology, 538 
symptoms, 539 
treatment, 543 
hemorrhagic, chronic, 547 
treatment, 543 
tubercular, acute, 548 
chronic, 549 

Pertussis. See Whooping-cough. 

Petit mal, 865 

Pharyngitis complicating rheumatism, 
673 

Phosphaturia, 622 

Phthisis florida. See Phthisis, pulmo¬ 
nary, acute. 
pulmonary, acute, 328 

diagnosis, differential, 384 
pathology, 382 
pulmonary, chronic, 386 
complications, 394 
pathology, 386 
physical signs, 393 
symptoms, 388 
treatment, 395 

Pia mater, cerebral, diseases of, 739 
spinal, diseases of, 790 
Pin-worms, 911 
Plasmodium malarise, 152 
Pleura, diseases of, 400 
new growths of, 424 
Pleurisy, chronic, 416 


Pleurisy, chronic, course and diagno¬ 
sis, 418 

symptoms and physical signs, 417 
treatment, 418 

complicating lobar pneumonia, 336 
effusion in, mechanical effects of, 404 
fibrinous or dry, 400 
plastic, 400 

pathology and symptoms, 401 
physical signs, 402 
prognosis and treatment, 403 
purulent, 411 
course, 414 
pathology, 412 
prognosis, 415 
symptoms, 413 
treatment, 415 
tubercular, 418 
with effusion, 403 
course, 409 
sequela?, 409 
symptoms, 404 
treatment, 410 

Pneumogastric nerve, diseases of, 840 
Pneumonia, broncho-, 341 

catarrhal. See Broncho-pneumonia. 
complicating epidemic influenza, 91 
interstitial, 352 

prognosis and treatment, 355 
symptoms, 354 
lobar, 324 

complications, 336 
etiology, 325 
pathology, 326 
physical signs, 333 
symptoms, 328 
cerebral, 332 
treatment, 339 

lobular. See Broncho-pneumonia . 
prognosis, 338 
syphilitic fibroid, 366 
Pneumopericardium, 197, 198 
Pneumothorax, 420 
diagnosis, 423 
symptoms, 421 
treatment, 424 
Podagra, 678 

Poliomyelitis, anterior, acute, 797 
in adults, 802 
in children, 798 
pathology, 798 
symptoms, 799 
treatment, 801 




INDEX. 931 


Poliomyelitis, subacute and chronic, 
803 

Polyneuritis, acute febrile, 851 
Portal vein, obstruction of, chronic, 603 
thrombosis of, 604 
Pox. See Syphilis. 

Pseudo-angina, 269, 270 
Pseudo-leukaemia, 727 
anaemia in, 729 
diagnosis, 730 
etiology and pathology, 727 
glandular swellings in, 729 
symptoms, 728 
treatment, 730 
Pseudo-rabies, 168 
Pseudo-rheumatism, 675 
Pulmonary affections complicating 
rheumatism, 671 
regurgitation, 242 
stenosis, 243 

Purpura, fulminating, 706 
hcemorrhagica, 706 
acute, 706 
subacute, 707 
rheiunatica, 705 
symptomatic, 705 
Purpuric diseases, 704 
treatment, 709 

Pustule, malignant. See Anthrax. 
Pyaemia, 121 
arterial, 122 
definition, 121 
diagnosis, 123 
etiology, 122 
idiopathic, 122 
prognosis, 123 
symptoms, 123 
treatment, 124 
Pyelitis, 656 

Pyelonephritis, tubercular, 648 
Pyo-pneumothorax, 420 

subphrenic. See Perihepatitis , 

acute. 

Pyrosis, 447 
Pyuria, 621 

Quinine in treatment of epidemic in¬ 
fluenza, 92 

of malarial fever, 161 

Rabies. See Hydrophobia. 

pseudo-, 168. 

Rachitis, 701 


Rales, pleural and bronchial, differen¬ 
tial diagnosis, 402 
Raynaud’s disease, 899 
Rectum, cancer of, 522 

physical examination, 523 
prognosis and treatment, 524 
Regurgitation, aortic, 234 
pulmonary, 242 
tricuspid, 241 
Relapsing fever, 51 
complications, 54 
convalescence from, 54 
definition and synonyms, 51 
etiology, 52 
exciting cause, 52 
pathology, 52 
prognosis, 54 
symptoms, 53 
treatment, 54 

Ren mobilis. See Kidney, movable. 
Respiratory system, diseases of, 292 
Rheumatic fever, 667 
Rheumatism, articular, acute, 667 
complications, 670 
etiology, 667 

inflammation of serous mem¬ 
branes in, 669 
symptoms, 668 

theories as to causation of, 667 
treatment, 673 
chronic, 675 

pathology and symptoms, 676 
treatment, 677 
cerebral, 672 
muscular, 677 
treatment, 678 
pseudo-, 675 
secondary, 675 
Rheumatisme fibreux, 676 
Rickets, 701 

etiology and pathology, 701 
symptoms, 702 
treatment, 704 
Roseola. See Rubella. 

Rotheln. See Rubella. 

Rubella, 81 
eruption of, 82 
etiology and synonyms, 81 
prognosis, 82 
symptoms, 82 
treatment, 82 
Rubeola. See Measles. 

Rumination, 480 




93 2 


INDEX. 


Sapr^mia, 125 

Scarlatina. See Scarlet fever. 

Scarlet fever, 66 

and diphtheria, relation between, 
67 

angina cases, 72 
complicating inflammations, 68 
complications, 72 

kidneys, lesions of, 72 
muscles, inflammation of, 74 
serous membranes, inflamma¬ 
tion of, 74 

definition and synonyms, 66 

desquamation, 70 

eruption of, 69 

etiology, 67 

hemorrhagic cases, 71 

malignant cases, 71 

mild and rudimentary cases, 70 

pathology, 68 

prognosis, 74 

severe and prolonged cases, 71 
susceptibility to, 67 
symptoms, 68 
treatment, 74 

variations from regular course, 70 
Schonlein’s disease, 705 
Sciatica, 858 
Sclerema, 904 
Scleroderma, 904 
Sclerosis, amyotrophic lateral, 807 
cerebro-spinal, 781 
lateral, 810 
primary, 810 
secondary, 811 

posterior spinal. See Loco?notor 
ataxia. 

Scorbutus, 698 
Scrofula, 733 
Scurvy, 698 
in children, 699 
Sepsis. See Septiccemia. 
acute peritoneal, 537 
peritoneal, treatment, 543 
Septicaemia, clinical forms, 124 
definition and synonym, 124 
progressive, 126 
Seventh nerve, diseases of, 835 
Sinuses, venous, thrombosis of, 760 
Sixth nerve, diseases of, 834 
Small-pox, 55 

complications and sequelae, 61 
confluent form, 59 


Small-pox, contagiousness of, 55 
definition and synonym, 55 
discrete form, 56 

stage of eruption, 57 
stage of invasion, 56 
etiology, 55 
hemorrhagic form, 60 
malignant form, 60 
pathology, 56 
prognosis, 62 
susceptibility to, 55 
symptoms, 56 
treatment, 62 
varioloid, 61 

Spasm, habit- , 879 

Spinal accessory nerve, diseases of, 
844 

cord, blood-vessels of, anaemia of, 

794 

diseases of, 794 
hyperaemia of, 794 
diseases of, 788 

embolism and thrombosis of, 796 
hemorrhage into, 795 
symptoms resulting from acute de¬ 
struction of anterior cornua 
of, 798 

tumors of, 830 

membranes, hemorrhage into, 793 

Spirillum fever. See Relapsing fever. 

Splenic fever. See Anthrax. 

St. Vitus’s dance. See Chorea. 

; Steam-tent in treatment of diphtheria, 
H4 

Stenocardia. See Angina pectoris. 

Stenosis, aortic, 239 
mitral, 230 
pulmonary, 243 
tricuspid, 242 

Stomach, atrophy of. See Gastritis , 
chronic catarrhal. 
cancer of, 464 
etiology, 464 
pathology, 464 

peculiarities in the clinical course, 
470 

physical examination in, 469 
prognosis, 471 
symptoms, 466 
constitutional, 469 
gastric, 466 

of secondary growths, 469 
dilatation of, 452 








INDEX. 


933 


Stomach, dilatation of, pathology, 452 
physical signs, 454 
prognosis, 455 
symptoms, 453 
treatment, 465 
diseases of, 440 
hemorrhage from, 472 
diagnosis, 474 
etiology, 472 
symptoms, 473 
treatment, 475 
neuroses of, 475 

dyspepsia, nervous, 475 
gastralgia, gastrodynia, 477 
hypersecretion and hyperacidity, 
476 

peristaltic unrest, 480 
rumination, 480 
vomiting, nervous, 479 
tumors of, non-cancerous, 471 
ulcer of, 456 
etiology, 456 
pathogenesis, 459 
pathology, 457 

sequelae and complications, 458 
symptoms, 460 
treatment, 462 

varieties in clinical course, 461 
Strongylus duodenalis, 912 
Stupor, syphilitic, 787 
Sun-stroke, 895 
Syncope, local, 899 
Syphilides, late, 141 
Syphilis, 137 
acquired, 138 
periods of, 138 
prognosis, 142 

symptoms of primary stage, 138 
of secondary stage, 139 
of tertiary stage, 141 
treatment, curative, 143 
prophylactic, 142 
hereditary, 145 
etiology, 145 
symptoms, 146 
treatment, 147 

tertiary, amyloid degeneration fol¬ 
lowing, 142 
Syringo-myelia, 828 

Tabes dorsalis. See Locomotor 
ataxia. 

mesenterica, 735 


Tachycardia, 263 
Taenia mediocanellata, 916 
saginata, 916 
solium, 915 
Taeniae, 915 
Tape-worms, 915 
Tetanilla, 880 
Tetanus, 169 
bacillus of, 169 
definition and synonyms, 169 
diagnosis, 171 
duration, 171 
etiology, 169 
hydrophobic, 171 
pathology, 170 
prognosis, 172 
symptoms, 170 
treatment, 172 
Tetany, 880 
Thermic fever, 896 
Third nerve, diseases of, 832 
Thomsen’s disease, 909 
Thread-worms, 911 
Thymus gland, diseases of, 431 
Thyroid-feeding in treatment of myx- 
cedema, 903 
Tic convulsif, 879 
douloureux, 834, 857 
simple, 879 
Torticollis, 845 
spasmodic, 845 
Trematodes, 910 
Tremor cordis, 262 
Trichina spiralis, 913 
Trichinosis, 913 
Trichocephalus dispar, 912 
Tricuspid regurgitation, 241 
stenosis, 242 

Trismus, 834. See also Tetanus. 
Tuberculosis, miliary, acute, 148 
definition, 148 
diagnosis, 152 
etiology, 148 
pathology, 148 
prognosis, 152 
symptoms, general, 149 
local, 150 
treatment, 152 
types of the disease, 151 
pulmonary, acute, 373 
diagnosis, 376 
pathology, 374 
physical signs, 375 






934 INDEX. 


Tuberculosis, pulmonary, acute, prog¬ 
nosis, 377 
symptoms, 374 
treatment, 395 
chronic, 377 
course, 379 
physical signs, 379 
prognosis, 381 
symptoms, 378, 381 
treatment, 395 
treatment, 395 
creosote in, 398 
Koch’s lymph in, 398 
prophylactic, 395 
to arrest the disease, 396 
to relieve symptoms, 399 
Tumors of the stomach, non-cancerous, 
47i 

Typhoid fever, 17 

catarrhal or croupous enteritis in, 
22 

changes in the intestinal lymphcki 
tissue in, 21 

in the mesenteric glands in, 22 
complicating lesions, 22 
complications, 35 
convalescence from, 38 
treatment during, 45 
course, 32 

definition and synonyms, 17 

diet in, 40 

eruption of, 31 

essential lesions, 21 

etiology, 17 

exciting cause, 18 

heart-muscle in, 23 

in children. 34 

insidious cases of, 34 

in the aged, 35 

kidneys in, 23 

larynx in, 23 

liver in, 23 

lungs in, 23 

methods of infection, 19 
parotitis in, 23 
pathology, 20 
peritonitis in, 22 
personal susceptibility to, 18 
pharynx in, 23 
prognosis, 38 
pulse in, 26 

relapses and recrudescences, 37 
spleen in, 22, 30 


Typhoid fever, symptoms, 23 
fever, 24 

gastro-intestinal, 26 
nervous, 29 
pulse, 26 
treatment, 39 

Brand’s method, 42 

contraindications to em¬ 
ployment of, 42 
during convalescence, 45 
general management, 40 
internal antipyretics in, 43 
medical, 41 
modified baths, 43 
of recrudescences, 46 
prophylactic, 39 
stimulants in, 44 
wet pack in, 43 
urine in, 31 
Typhus fever, 46 

complications, 50 
convalescence from, 50 
crisis in, 50 

definition and synonyms, 46 
eruption in, 48 
etiology, 46 
pathology, 47 
prognosis, 50 
symptoms, 47 
cerebral, 49 
temperature in, 47 
treatment, 51 

Ulcer, peptic. See Stomach, ulcer of. 
Unrest, peristaltic, 479 
Uric acid, daily excretion of, 622 
Uricsemia, 622 

Urinary secretion, anomalies of, 614 
Urine, acetone in, 625 

albumin in, Heller’s test for, 616 
blood in, Heller’s test for, 618 
changes in, in chronic Bright’s 
disease, 637, 641 
chyle in, 624 

diminished, in acute degeneration 
of the kidneys, 628 
in congestion of the kidneys, 
626, 627 

in movable kidney, 613 
fat in, 625 
haemoglobin in, 619 
in acute exudative nephritis, 630, 
631 



index ; 935 


Urine in acute yellow atrophy of the 
liver, 562 

in diabetes mellitus, 693 
indigo in, 624 
in gout, 683 
in jaundice, 591 

in tubercular pyelonephritis, 648 
in waxy degeneration of the kid¬ 
neys, 647 

oxalate of lime in, 624 
peptone in, 621 
phosphates in, 622 
pus in, 621 

quantity of, in chronic degeneration 
of the kidneys, 629 
uric acid in, 622 
Urticaria, giant, 900 

Vaccination. See Vaccinia. 

complications of, 65 
Vaccinia, 64 

Valvular disease. See Endocarditis, 
chronic. 

Varicella, 65 

definition and synonym, 65 
eruption of, 66 
etiology, 65 
prognosis, 66 
symptoms, 65 
treatment, 66 
Variola. See Small-pox. 

Varioloid, 61 

Vaso-motor and trophic disorders, 899 
Vertigo, auditory, 839 
labyrinthine, 839 

Vomiting in acute peritonitis, 540 


Vomiting in cancer of the stomach, 467 
in cholelithiasis, 597 
in intestinal obstruction, 528 
nervous, 479 

Water-brasii, 447 
Weil’s disease, 181 
Werlhoff’s disease, 706 
Westphal’s symptom, 815 
Whip-worm, 912 
Whooping-cough, 85 

complications and sequela;, 87 
definition and synonym, 85 
etiology, 85 
lesion, 85 
symptoms, 85 
treatment, 87 
local, 88 

Woolsorter’s disease. See Anthrax. 
Wrist-drop, 851 
Writer’s cramp, 884 
Wry-neck, 845 

Yellow fever, 133 

complications and sequelae, 136 
contagiousness of, 134 
definition, 133 
diagnosis, 136 
etiology, 133 
immunity from, 134 
incubation, 134 
pathology, 134 
prognosis, 136 
symptoms, 134 
treatment, general, 137 
prophylactic, 136 












































































































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